Independent effects of volume and energy density manipulation on energy intake and appetite in healthy adults: A randomized, controlled, crossover study.

Consuming enough energy to meet high energy demands can be challenging for military personnel wherein logistical constraints limit food availability. Increasing dietary energy density (ED) and/or volume density (VD) of rations may be countermeasures, but whether positive linear associations between ED and energy intake (EI) hold at moderate-to-high ED and VD is unclear. This study examined the effects of covertly increasing the ED and VD of moderate ED (≥1.6 kcal/g) foods on appetite and energy intake. Twenty healthy men completed four 2-day treatments in random order by consuming a standardized diet containing three experimental food items (EXP) engineered using leavening, physical compression and fat manipulation to be isovolumetric but lower (L) or higher (H) in ED and VD creating four treatments: LED/LVD, LED/HVD, HED/LVD, HED/HVD. Consumption of EXP was compulsory during two meals and a snack, but remaining intake was self-selected (SSF). Results failed to show any ED-by-VD interactions. During LVD, EI was lower for EXP (-417 kcal [95%CI: 432, -402], p < 0.01) and TOTAL (SSF + EXP) (-276 kcal [95%CI: 470, -83], p = 0.01) compared to HVD, while SSF EI did not differ (140 kcal [-51, 332], p = 0.15). During LED, EI for EXP (-291 kcal [95%CI: 306, -276], p < 0.01) was lower than HED, while SSF EI was higher than HED (203 kcal 95%CI: [12, 394], p = 0.04) and TOTAL EI did not differ (-88 kcal [-282, 105], p = 0.36). Thus, when a small isovolumetric portion of the diet was manipulated, increasing the VD of moderate ED foods failed to elicit compensatory reductions in ad libitum EI while increasing the ED of moderate ED foods did. Findings may support VD manipulation of moderate ED foods as a strategy to promote increased short-term EI in environments wherein logistical burden may limit food volume.

Orally Ingested Probiotic, Prebiotic, and Synbiotic Interventions as Countermeasures for Gastrointestinal Tract Infections in Nonelderly Adults: A Systematic Review and Meta-Analysis.

Meta-analyses have not examined the prophylactic use of orally ingested probiotics, prebiotics, and synbiotics for preventing gastrointestinal tract infections (GTIs) of various etiologies in adult populations, despite evidence that these gut microbiota-targeted interventions can be effective in treating certain GTIs. This systematic review and meta-analysis aimed to estimate the effects of prophylactic use of orally ingested probiotics, prebiotics, and synbiotics on GTI incidence, duration, and severity in nonelderly, nonhospitalized adults. CENTRAL, PubMed, Scopus, and Web of Science were searched through January 2022. English-language, peer-reviewed publications of randomized, placebo-controlled studies testing an orally ingested probiotic, prebiotic, or synbiotic intervention of any dose for ≥1 wk in adults who were not hospitalized, immunosuppressed, or taking antibiotics were included. Results were analyzed using random-effects meta-analyses of intention-to-treat (ITT) and complete case (CC) cohorts. Heterogeneity was explored by subgroup meta-analysis and meta-regression. The risk of bias was assessed using the Cochrane risk-of-bias 2 tool. Seventeen publications reporting 20 studies of probiotics (n = 16), prebiotics (n = 3), and synbiotics (n = 1) were identified (n > 6994 subjects). In CC and ITT analyses, risk of experiencing ≥1 GTI was reduced with probiotics (CC analysis-risk ratio: 0.86; 95% CI: 0.73, 1.01) and prebiotics (risk ratio: 0.80; 95% CI: 0.66, 0.98). No effects on GTI duration or severity were observed. Sources of heterogeneity included the study population and number of probiotic strains administered but were often unexplained, and a high risk of bias was observed for most studies. The specific effects of individual probiotic strains and prebiotic types could not be assessed owing to a lack of confirmatory studies. Findings indicated that both orally ingested probiotics and prebiotics, relative to placebo, demonstrated modest benefit for reducing GTI risk in nonelderly adults. However, results should be interpreted cautiously owing to the low number of studies, high risk of bias, and unexplained heterogeneity that may include probiotic strain-specific or prebiotic-specific effects. This review was registered at PROSPERO as CRD42020200670.

Severe, short-term sleep restriction reduces gut microbiota community richness but does not alter intestinal permeability in healthy young men.

Sleep restriction alters gut microbiota composition and intestinal barrier function in rodents, but whether similar effects occur in humans is unclear. This study aimed to determine the effects of severe, short-term sleep restriction on gut microbiota composition and intestinal permeability in healthy adults. Fecal microbiota composition, measured by 16S rRNA sequencing, and intestinal permeability were measured in 19 healthy men (mean ± SD; BMI 24.4 ± 2.3 kg/m2, 20 ± 2 years) undergoing three consecutive nights of adequate sleep (AS; 7-9 h sleep/night) and restricted sleep (SR; 2 h sleep/night) in random order with controlled diet and physical activity. α-diversity measured by amplicon sequencing variant (ASV) richness was 21% lower during SR compared to AS (P = 0.03), but α-diversity measured by Shannon and Simpson indexes did not differ between conditions. Relative abundance of a single ASV within the family Ruminococcaceae was the only differentially abundant taxon (q = 0.20). No between-condition differences in intestinal permeability or ß-diversity were observed. Findings indicated that severe, short-term sleep restriction reduced richness of the gut microbiota but otherwise minimally impacted community composition and did not affect intestinal permeability in healthy young men.

Carbohydrate intake in recovery from aerobic exercise differentiates skeletal muscle microRNA expression.

Posttranscriptional regulation by microRNA (miRNA) facilitates exercise and diet-induced skeletal muscle adaptations. However, the impact of diet on miRNA expression during postexercise recovery remains unclear. The objective of this study was to examine the effects of consuming carbohydrate or a nutrient-free control on skeletal muscle miRNA expression during 3 h of recovery from aerobic exercise. Using a randomized, crossover design, seven men (means ± SD, age: 21 ± 3 yr; body mass: 83 ± 13 kg; V̇o2peak: 43 ± 2 mL/kg/min) completed two-cycle ergometry glycogen depletion trials followed by 3 h of recovery while consuming either carbohydrate (CHO: 1 g/kg/h) or control (CON: nutrient free). Muscle biopsy samples were obtained under resting fasted conditions at baseline and at the end of the 3-h recovery (REC) period. miRNA expression was determined using unbiased RT-qPCR microarray analysis. Trials were separated by 7 days. Twenty-five miRNAs were different (P < 0.05) between CHO and CON at REC, with Let7i-5p and miR-195-5p being the most predictive of treatment. In vitro overexpression of Let7i-5p and miR-195-p5 in C2C12 skeletal muscle cells decreased (P < 0.05) the expression of protein breakdown (Foxo1, Trim63, Casp3, and Atf4) genes, ubiquitylation, and protease enzyme activity compared with control. Energy sensing (Prkaa1 and Prkab1) and glycolysis (Gsy1 and Gsk3b) genes were lower (P < 0.05) with Let7i-5p overexpression compared with miR-195-5p and control. Fat metabolism (Cpt1a, Scd1, and Hadha) genes were lower (P < 0.05) in miR-195-5p than in control. These data indicate that consuming CHO after aerobic exercise alters miRNA profiles compared with CON, and these differences may govern mechanisms facilitating muscle recovery.NEW & NOTEWORTHY Results provide novel insight into effects of carbohydrate intake on the expression of skeletal muscle microRNA during early recovery from aerobic exercise and reveal that Let7i-5p and miR-195-5p are important regulators of skeletal muscle protein breakdown to aid in facilitating muscle recovery.

Serum Branched-Chain Amino Acid Metabolites Increase in Males When Aerobic Exercise Is Initiated with Low Muscle Glycogen.

This study used global metabolomics to identify metabolic factors that might contribute to muscle anabolic resistance, which develops when aerobic exercise is initiated with low muscle glycogen using global metabolomics. Eleven men completed this randomized, crossover study, completing two cycle ergometry glycogen depletion trials, followed by 24 h of isocaloric refeeding to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate 1.0 g/kg fat) glycogen. Participants then performed 80 min of cycling (64 ± 3% VO2 peak) while ingesting 146 g carbohydrate. Serum was collected before glycogen depletion under resting and fasted conditions (BASELINE), and before (PRE) and after (POST) exercise. Changes in metabolite profiles were calculated by subtracting BASELINE from PRE and POST within LOW and AD. There were greater increases (p < 0.05, Q < 0.10) in 64% of branched-chain amino acids (BCAA) metabolites and 69% of acyl-carnitine metabolites in LOW compared to AD. Urea and 3-methylhistidine had greater increases (p < 0.05, Q < 0.10) in LOW compared to AD. Changes in metabolomics profiles indicate a greater reliance on BCAA catabolism for substrate oxidation when exercise is initiated with low glycogen stores. These findings provide a mechanistic explanation for anabolic resistance associated with low muscle glycogen, and suggest that exogenous BCAA requirements to optimize muscle recovery are likely greater than current recommendations.

Initiating aerobic exercise with low glycogen content reduces markers of myogenesis but not mTORC1 signaling.

BACKGROUND: The effects of low muscle glycogen on molecular markers of protein synthesis and myogenesis before and during aerobic exercise with carbohydrate ingestion is unclear. The purpose of this study was to determine the effects of initiating aerobic exercise with low muscle glycogen on mTORC1 signaling and markers of myogenesis. METHODS: Eleven men completed two cycle ergometry glycogen depletion trials separated by 7-d, followed by randomized isocaloric refeeding for 24-h to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate, 1.0 g/kg fat) glycogen. Participants then performed 80-min of cycle ergometry (64 ± 3% VO2peak) while ingesting 146 g carbohydrate. mTORC1 signaling (Western blotting) and gene transcription (RT-qPCR) were determined from vastus lateralis biopsies before glycogen depletion (baseline, BASE), and before (PRE) and after (POST) exercise. RESULTS: Regardless of treatment, p-mTORC1Ser2448, p-p70S6KSer424/421, and p-rpS6Ser235/236 were higher (P < 0.05) POST compared to PRE and BASE. PAX7 and MYOGENIN were lower (P < 0.05) in LOW compared to AD, regardless of time, while MYOD was lower (P < 0.05) in LOW compared to AD at PRE, but not different at POST. CONCLUSION: Initiating aerobic exercise with low muscle glycogen does not affect mTORC1 signaling, yet reductions in gene expression of myogenic regulatory factors suggest that muscle recovery from exercise may be reduced.

Severe sleep restriction suppresses appetite independent of effects on appetite regulating hormones in healthy young men without obesity.

OBJECTIVE: Several nights of moderate (4-5 hr/night) sleep restriction increases appetite and energy intake, and may alter circulating concentrations of appetite regulating hormones. Whether more severe sleep restriction has similar effects is unclear. This study aimed to determine the effects of severe, short-term sleep restriction on appetite, ad libitum energy intake during a single meal, appetite regulating hormones, and food preferences. METHODS: Randomized, crossover study in which 18 healthy men (mean ± SD: BMI 24.4 ± 2.3 kg/m2, 20 ± 2 yr) were assigned to three consecutive nights of sleep restriction (SR; 2 hr sleep opportunity/night) or adequate sleep (AS; 7-9 hr sleep opportunity/night) with controlled feeding and activity designed to maintain energy balance throughout the 3-day period. On day 4, participants consumed a standardized breakfast. Appetite, assessed by visual analogue scales, and circulating ghrelin, peptide-YY (PYY), glucagon-like peptide (GLP-1), insulin, and glucose concentrations were measured before and every 20-60 min for 4hr after the meal. Ad libitum energy and macronutrient intakes were then measured at a provided buffet lunch. Food preferences were measured by Leeds Food Preference Questionnaire (LFPQ) administered before and after the lunch. RESULTS: Area under the curve (AUC) of postprandial hunger (-23%), desire to eat (-23%), and prospective consumption (-18%) ratings were all lower, and postprandial fullness AUC (25%) was higher after SR relative to after AS (p ≤ 0.02). Ad libitum energy intake at the lunch meal was 332 kcal [95% CI: -479, -185] (p<0.001) lower after SR relative to after AS, but relative macronutrient intakes and LFPQ scores did not differ. Postprandial glucose, insulin, PYY, GLP-1, and ghrelin AUCs did not differ between phases. However, mean concentrations of PYY (-11%) and GLP-1 (-4%) over the 4-hr testing period were lower, and glucose concentrations were 6% higher, after SR relative to after AS (p ≤ 0.01). CONCLUSION: In contrast with reported effects of moderate sleep restriction, severe sleep restriction reduced appetite and energy intake, had no impact food preferences, and had little impact on appetite regulating hormones. Findings suggest that severe sleep restriction may suppress appetite and food intake, at least at a single meal, by a mechanism independent of changes in food preference or appetite regulating hormones.

Acute hypoxia reduces exogenous glucose oxidation, glucose turnover, and metabolic clearance rate during steady-state aerobic exercise.

BACKGROUND: Exogenous carbohydrate oxidation is lower during steady-state aerobic exercise in native lowlanders sojourning at high altitude (HA) compared to sea level (SL). However, the underlying mechanism contributing to reduction in exogenous carbohydrate oxidation during steady-state aerobic exercise performed at HA has not been explored. OBJECTIVE: To determine if alterations in glucose rate of appearance (Ra), disappearance (Rd) and metabolic clearance rate (MCR) at HA provide a mechanism for explaining the observation of lower exogenous carbohydrate oxidation compared to during metabolically-matched, steady-state exercise at SL. METHODS: Using a randomized, crossover design, native lowlanders (n = 8 males, mean ±â€¯SD, age: 23 ±â€¯2 yr, body mass: 87 ±â€¯10 kg, and VO2peak: SL 4.3 ±â€¯0.2 L/min and HA 2.9 ±â€¯0.2 L/min) consumed 145 g (1.8 g/min) of glucose while performing 80-min of metabolically-matched (SL: 1.66 ±â€¯0.14 V̇O2 L/min 329 ±â€¯28 kcal, HA: 1.59 ±â€¯0.10 V̇O2 L/min, 320 ±â€¯19 kcal) treadmill exercise in SL (757 mmHg) and HA (460 mmHg) conditions after a 5-h exposure. Substrate oxidation rates (g/min) and glucose turnover (mg/kg/min) during exercise were determined using indirect calorimetry and dual tracer technique (13C-glucose oral ingestion and [6,6-2H2]-glucose primed, continuous infusion). RESULTS: Total carbohydrate oxidation was higher (P < 0.05) at HA (2.15 ±â€¯0.32) compared to SL (1.39 ±â€¯0.14). Exogenous glucose oxidation rate was lower (P < 0.05) at HA (0.35 ±â€¯0.07) than SL (0.44 ±â€¯0.05). Muscle glycogen oxidation was higher at HA (1.67 ±â€¯0.26) compared to SL (0.83 ±â€¯0.13). Total glucose Ra was lower (P < 0.05) at HA (12.3 ±â€¯1.5) compared to SL (13.8 ±â€¯2.0). Exogenous glucose Ra was lower (P < 0.05) at HA (8.9 ±â€¯1.3) compared to SL (10.9 ±â€¯2.2). Glucose Rd was lower (P < 0.05) at HA (12.7 ±â€¯1.7) compared to SL (14.3 ±â€¯2.0). MCR was lower (P < 0.05) at HA (9.0 ±â€¯1.8) compared to SL (12.1 ±â€¯2.3). Circulating glucose and insulin concentrations were higher in response carbohydrate intake during exercise at HA compared to SL. CONCLUSION: Novel results from this investigation suggest that reductions in exogenous carbohydrate oxidation at HA may be multifactorial; however, the apparent insensitivity of peripheral tissue to glucose uptake may be a primary determinate.

Glycaemic regulation, appetite and ex vivo oxidative stress in young adults following consumption of high-carbohydrate cereal bars fortified with polyphenol-rich berries.

Consumption of certain berries appears to slow postprandial glucose absorption, attributable to polyphenols, which may benefit exercise and cognition, reduce appetite and/or oxidative stress. This randomised, crossover, placebo-controlled study determined whether polyphenol-rich fruits added to carbohydrate-based foods produce a dose-dependent moderation of postprandial glycaemic, glucoregulatory hormone, appetite and ex vivo oxidative stress responses. Twenty participants (eighteen males/two females; 24 (sd 5) years; BMI: 27 (sd 3) kg/m2) consumed one of five cereal bars (approximately 88 % carbohydrate) containing no fruit ingredients (reference), freeze-dried black raspberries (10 or 20 % total weight; LOW-Rasp and HIGH-Rasp, respectively) and cranberry extract (0·5 or 1 % total weight; LOW-Cran and HIGH-Cran), on trials separated by ≥5 d. Postprandial peak/nadir from baseline (Δmax) and incremental postprandial AUC over 60 and 180 min for glucose and other biochemistries were measured to examine the dose-dependent effects. Glucose AUC0-180 min trended towards being higher (43 %) after HIGH-Rasp v. LOW-Rasp (P=0·06), with no glucose differences between the raspberry and reference bars. Relative to reference, HIGH-Rasp resulted in a 17 % lower Δmax insulin, 3 % lower C-peptide (AUC0-60 min and 3 % lower glucose-dependent insulinotropic polypeptide (AUC0-180 min) P<0·05. No treatment effects were observed for the cranberry bars regarding glucose and glucoregulatory hormones, nor were there any treatment effects for either berry type regarding ex vivo oxidation, appetite-mediating hormones or appetite. Fortification with freeze-dried black raspberries (approximately 25 g, containing 1·2 g of polyphenols) seems to slightly improve the glucoregulatory hormone and glycaemic responses to a high-carbohydrate food item in young adults but did not affect appetite or oxidative stress responses at doses or with methods studied herein.

Exercising with low muscle glycogen content increases fat oxidation and decreases endogenous, but not exogenous carbohydrate oxidation.

BACKGROUND: Initiating aerobic exercise with low muscle glycogen content promotes greater fat and less endogenous carbohydrate oxidation during exercise. However, the extent exogenous carbohydrate oxidation increases when exercise is initiated with low muscle glycogen is unclear. PURPOSE: Determine the effects of muscle glycogen content at the onset of exercise on whole-body and muscle substrate metabolism. METHODS: Using a randomized, crossover design, 12 men (mean ±â€¯SD, age: 21 ±â€¯4 y; body mass: 83 ±â€¯11 kg; VO2peak: 44 ±â€¯3 mL/kg/min) completed 2 cycle ergometry glycogen depletion trials separated by 7-d, followed by a 24-h refeeding to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate, 1.0 g/kg fat) glycogen stores. Participants then performed 80 min of steady-state cycle ergometry (64 ±â€¯3% VO2peak) while consuming a carbohydrate drink (95 g glucose +51 g fructose; 1.8 g/min). Substrate oxidation (g/min) was determined by indirect calorimetry and 13C. Muscle glycogen (mmol/kg dry weight), pyruvate dehydrogenase (PDH) activity, and gene expression were assessed in muscle. RESULTS: Initiating steady-state exercise with LOW (217 ±â€¯103) or AD (396 ±â€¯70; P < 0.05) muscle glycogen did not alter exogenous carbohydrate oxidation (LOW: 0.84 ±â€¯0.14, AD: 0.87 ±â€¯0.16; P > 0.05) during exercise. Endogenous carbohydrate oxidation was lower and fat oxidation was higher in LOW (0.75 ±â€¯0.29 and 0.55 ±â€¯0.10) than AD (1.17 ±â€¯0.29 and 0.38 ±â€¯0.13; all P < 0.05). Before and after exercise PDH activity was lower (P < 0.05) and transcriptional regulation of fat metabolism (FAT, FABP, CPT1a, HADHA) was higher (P < 0.05) in LOW than AD. CONCLUSION: Initiating exercise with low muscle glycogen does not impair exogenous carbohydrate oxidative capacity, rather, to compensate for lower endogenous carbohydrate oxidation acute adaptations lead to increased whole-body and skeletal muscle fat oxidation.