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Background: To examine associations between body composition and vitamin D status in children participating in a lifestyle intervention. Methods: Children (6–12 y, n = 101) with a body mass index (BMI)-for-age >85th percentile were randomized to six dietitian-led behavior counselling sessions or no intervention. Plasma 25-hydroxyvitamin D (25(OH)D), anthropometry, and body composition using dual-energy X-ray absorptiometry were assessed every 3 months for 1 year. For each anthropometry variable (z-scores), tertiles were created to test for differences in 25(OH)D over time (tertile-by-time), and for changes in the z-score (loss, maintain, gain)-by-time, and according to fat patterning (android vs. gynoid) using mixed effects models. Results: The baseline plasma 25(OH)D was 62.2 nmol/L (95%CI: 58.7–65.7), and none < 30 nmol/L. At 6 mo, children with gynoid fat patterning had higher 25(OH)D concentrations than in those with android fat patterning (64.5 ± 1.1 nmol/L vs. 50.4 ± 1.0 nmol/L, p < 0.003, Cohen’s f = 0.20). Children with the lowest lean mass index z-score at 9 mo had higher plasma 25(OH)D concentrations than children with the highest z-score at baseline, 3 mo, and 6 mo (p < 0.05, Cohen’s f = 0.20). No other significant differences were observed. Conclusion: In this longitudinal study, vitamin D deficiency was not present in children 6–12 y of age with obesity. Reductions in adiposity did not alter the vitamin D status.

High-intensity exercise inhibits appetite, in part, via alterations in the peripheral concentrations of the appetite-regulating hormones acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and active peptide tyrosine-tyrosine (PYY). Given lactate may mediate these effects, we used sodium bicarbonate (NaHCO(3)) supplementation in a double-blind, placebo-controlled, crossover design to investigate lactate’s purported role in exercise-induced appetite suppression. Eleven males completed two identical high-intensity interval training sessions (10 × 1 min cycling bouts at ~90% heart rate maximum interspersed with 1-min recovery), where they ingested either NaHCO(3) (BICARB) or sodium chloride (NaCl) as a placebo (PLACEBO) preexercise. Blood lactate, acylated ghrelin, GLP-1, and PYY concentrations, as well as overall appetite were assessed preexercise and 0, 30, 60, and 90 min postexercise. Blood lactate was greater immediately (P < 0.001) and 30 min postexercise (P = 0.049) in the BICARB session with an increased (P = 0.009) area under the curve (AUC). The BICARB session had lower acylated ghrelin at 60 (P = 0.014) and 90 min postexercise (P = 0.016), with a decreased AUC (P = 0.039). The BICARB session had increased PYY (P = 0.034) with an increased AUC (P = 0.031). The BICARB session also tended (P = 0.060) to have increased GLP-1 at 30 (P = 0.003) and 60 min postexercise (P < 0.001), with an increased AUC (P = 0.030). The BICARB session tended (P = 0.059) to reduce overall appetite, although there was no difference in AUC (P = 0.149). These findings support a potential role for lactate in the high-intensity exercise-induced appetite-suppression. NEW & NOTEWORTHY We used sodium bicarbonate to increase lactate accumulation or sodium chloride as a placebo. Our findings further implicate lactate as a mediator of exercise-induced appetite suppression, given exercise-induced increases in lactate during the sodium bicarbonate session altered peripheral concentrations of appetite-regulating hormones, culminating in a reduction of appetite. This supports a lactate-dependent mechanism of appetite suppression following high-intensity exercise and highlights the potential of using lactate as a means of inducing a caloric deficit.

This study examines the involvement of two potential mechanisms (lactate and IL-6) that may explain the intensity-dependent effects of acute exercise on appetite-related parameters. Our findings support a clear intensity-dependent paradigm for appetite-regulation following exercise, as highlighted by the change in acylated ghrelin and the suppression of appetite and energy intake after vigorous exercise (continuous and intermittent). Further, our findings extend previous work in animal/cell models by providing evidence for the potential role of lactate and IL-6 in mediating changes in appetite-related parameters following exercise in humans., High-intensity exercise suppresses appetite partly through changes in peripheral appetite-regulating hormones. Lactate and IL-6 mediate the release of these hormones in animal/cell models and may provide a mechanistic link between exercise intensity and appetite regulation. The current study examined changes in appetite-regulating hormones, lactate, and IL-6 after different intensities of running. Eight males completed four experimental sessions: 1) moderate-intensity continuous training (MICT; 65% V̇o2max); 2) vigorous-intensity continuous training (VICT; 85% V̇o2max); 3) sprint interval training (SIT; repeated “all-out” sprints); and 4) Control (CTRL; no exercise). Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), total peptide YY (PYY), lactate, IL-6, and appetite perceptions were measured pre-, immediately postexercise, 30 min postexercise, and 90 min postexercise. Energy intake was recorded over 3 days. VICT and SIT suppressed ghrelin (P < 0.001), although SIT elicited a greater (P = 0.016 vs. MICT) and more prolonged (P < 0.001 vs. all sessions) response. GLP-1 increased immediately after MICT (P < 0.001) and 30 min after VICT (P < 0.001) and SIT (P < 0.002), while VICT elicited a greater postexercise increase in PYY vs. MICT (P = 0.027). Postexercise changes in blood lactate and IL-6 correlated with the area under the curve values for ghrelin (r = −0.60, P < 0.001) and GLP-1 (r = 0.42, P = 0.017), respectively. Appetite was suppressed after exercise (P < 0.001), although more so after VICT (P < 0.027) and SIT (P < 0.001) vs. MICT, and energy intake was reduced on the day after VICT (P < 0.017 vs. MICT and CTRL) and SIT (P = 0.049 vs. MICT). These findings support an intensity-dependent paradigm for appetite regulation following exercise and highlight the potential involvement of lactate and IL-6. NEW & NOTEWORTHY This study examines the involvement of two potential mechanisms (lactate and IL-6) that may explain the intensity-dependent effects of acute exercise on appetite-related parameters. Our findings support a clear intensity-dependent paradigm for appetite regulation following exercise, as highlighted by the change in acylated ghrelin and the suppression of appetite and energy intake after vigorous exercise (continuous and intermittent). Further, our findings extend previous work in animal/cell models by providing evidence for the potential role of lactate and IL-6 in mediating changes in appetite-related parameters following exercise in humans.

Background:Deterioration in bone health is a concern in managing pediatric inflammatory bowel diseases, but clear understanding of the independent contributions of disease and nutrition is lacking. This study aimed to ascertain whether bone health could be conserved during colitis by maintaining adequate nutritional intake in growing piglets.Methods:The effect of colitis on bone structure and strength was determined in piglets with dextran sulphate sodium-induced colitis. Piglets received either 100% macro/micronutrient requirements or 50% macro/100% micronutrient requirements. Femurs were analyzed for dual-energy x-ray absorptiometry, peripheral quantitative computed tomography, microcomputed tomography, and 3-point bending tests.Results:Colitis, regardless of a well-nourished or malnourished diet, compromised areal bone mineral density (−17%) and volumetric bone mineral density (−20%) in cortical and trabecular bone. Structural integrity at mid-diaphysis was maintained during colitis; however, lower cortical area, trabecular area, and bone mineral content resulted in lower energy to break.Conclusion:Colitis compromises both bone structure and strength of long bones in piglets, independent of macronutrient intakes. Although confirmation of these findings in pediatric cohorts is needed, these data identify aspects of bone health that may be affected by inflammatory bowel disease.

Sprint interval training (SIT) can elicit improvements in aerobic and anaerobic capacity. While variations in SIT protocols have been investigated, the influence of social processes cannot be overlooked. As research supports the use of groups to influence individual cognitions and behaviours, the current project assessed the effectiveness of a group-based intervention with participants conducting SIT. Specifically, 53 amateur athletes (age, 21.9 ± 2.9 years; 53% females) took part in a 4-week training program (3 sessions per week, 30-s “all-out” efforts with 4 min active recovery, repeated 4–6 times per session), and were assigned to “true group”, aggregate, or individual conditions. Results indicated no significant differences between groups for the physiological measures. With regards to training improvements from baseline for all participants— regardless of condition — significant main effects for time were identified for maximal oxygen uptake (2.5–2.8 mL·kg−1·min−1, p < 0.001, η2 = 0.03), time-trial performance (14–32 s, p < 0.001, η2 = 0.37), and anaerobic power (1.1–1.7 k·h−1, p < 0.001, η2 = 0.66). With regards to the psychological measures, significant main effects between groups were found for motivation (p = 0.033, η2 = 0.13), task self-efficacy (p = 0.018, η2 = 0.15), and scheduling self-efficacy (p = 0.003, η2 = 0.22). The true group experienced greater improvements in motivation than the individual condition, but the aggregate and individual conditions demonstrated greater increases in task and scheduling self-efficacy. Though the SIT paradigm employed induced training improvements similar to previous work, the group intervention was not able to further these improvements.

BackgroundChildhood obesity gives rise to health complications including impaired musculoskeletal development that associates with increased risk of fractures. Prevention and treatment programs should focus on nutrition education, increasing physical activity (PA), reducing sedentary behaviours, and should monitor bone mass as a component of body composition. To ensure lifestyle changes are sustained in the home environment, programs need to be family-centered. To date, no study has reported on a family-centered lifestyle intervention for obese children that aims to not only ameliorate adiposity, but also support increases in bone and lean muscle mass. Furthermore, it is unknown if programs of such nature can also favorably change eating and activity behaviors. The aim of this study is to determine the effects of a 1 y family-centered lifestyle intervention, focused on both nutrient dense foods including increased intakes of milk and alternatives, plus total and weight-bearing PA, on body composition and bone mass in overweight or obese children.Methods/designThe study design is a randomized controlled trial for overweight or obese children (6–8 y). Participants are randomized to control, standard treatment (StTx) or modified treatment (ModTx). This study is family-centred and includes individualized counselling sessions on nutrition, PA and sedentary behaviors occurring 4 weeks after baseline for 5 months, then at the end of month 8. The control group receives counselling at the end of the study. All groups are measured at baseline and every 3 months for the primary outcome of changes in body mass index Z-scores. At each visit blood is drawn and children complete a researcher-administered behavior questionnaire and muscle function testing. Changes from baseline to 12 months in body fat (% and mass), waist circumference, lean body mass, bone (mineral content, mineral density, size and volumetric density), dietary intake, self-reported PA and sedentary behaviour are examined.DiscussionThis family-centered theory-based study permits for biochemical and physiological assessments. This trial will assess the effectiveness of the intervention at changing lifestyle behaviours by decreasing adiposity while enhancing lean and bone mass. If successful, the intervention proposed offers new insights for the management or treatment of childhood obesity.Trial registrationClinicalTrials.gov,NCT01290016.