Accumulating exercise and postprandial health in adolescents

ArticleCopyright © 2015 Published by Elsevier Inc.Purpose: To examine the influence of exercise intensity on postprandial health outcomes in adolescents when exercise is accumulated throughout the day. Methods: 19 adolescents (9 male, 13.7 ± 0.4 y) completed three 1-day trials in a randomised order: 1) rest (CON); or four bouts of 2) 2 x 1 min cycling at 90% peak power with 75 s recovery (high-intensity interval exercise; HIIE); or 3) cycling at 90% of the gas exchange threshold (moderate-intensity exercise; MIE), which was work-matched to HIIE. Each bout was separated by 2 hours. Participants consumed a high fat milkshake for breakfast and lunch. Postprandial triacylglycerol (TAG), glucose, systolic blood pressure (SBP) and fat oxidation were assessed throughout the day. Results: There was no effect of trial on total area under the curve (TAUC) for TAG (P=0.87). TAUC-glucose was lower in HIIE compared to CON (P=0.03, ES=0.42) and MIE (P=0.04, ES=0.41), with no difference between MIE and CON (P=0.89, ES=0.04). Postprandial SBP was lower in HIIE compared to CON (P=0.04, ES=0.50) and MIE (P=0.04, ES=0.40), but not different between MIE and CON (P=0.52, ES=0.11). Resting fat oxidation was increased in HIIE compared to CON (P=0.01, ES=0.74) and MIE (P=0.05, ES=0.51), with no difference between MIE and CON (P=0.37, ES=0.24). Conclusion: Neither exercise trial attenuated postprandial lipaemia. However, accumulating brief bouts of HIIE, but not MIE, reduced postprandial plasma glucose and SBP, and increased resting fat oxidation in adolescent boys and girls. The intensity of accumulated exercise may therefore have important implications for health outcomes in youth.Sport and Health Sciences Research Committee, College of Life and Environmental Sciences, University of Exeter

Exercise intensity and the protection from postprandial vascular dysfunction in adolescents

This is the author accepted manuscript. The final version is available from American Physiological Society via the DOI in this recordBACKGROUND: Acute exercise transiently improves endothelial function, and protects the vasculature from the deleterious effects of a high fat meal (HFM). We sought to identify whether this response is dependent on exercise intensity in adolescents. METHODS: Twenty adolescents (10 male, 14.3 ± 0.3 y) completed three 1-day trials: 1) rest (CON); 2) 8x1 min cycling at 90% peak power with 75s recovery (high-intensity interval exercise; HIIE); 3) cycling at 90% of the gas exchange threshold (moderate-intensity exercise; MIE) one hour before consuming a HFM (1.50 g∙kg(-1) fat). Macrovascular and microvascular endothelial function were assessed before and immediately after exercise, and three hours after the HFM by flow mediated dilation (FMD) and laser Doppler imaging (peak reactive hyperaemia; PRH). RESULTS: FMD and PRH increased one hour after HIIE (P<0.001, ES=1.20 and P=0.048, ES=0.56) but were unchanged after MIE. FMD and PRH were attenuated three hours after the HFM in CON (P<0.001, ES=1.78 and P=0.02, ES=0.59). FMD remained greater three hours after the HFM in HIIE compared to MIE (P<0.001, ES=1.47) and CON (P<0.001, ES=2.54), and in MIE compared to CON (P<0.001, ES=1.40). Compared to CON, PRH was greater three hours after the HFM in HIIE (P=0.02, ES=0.71) and MIE (P=0.02, ES=0.84), with no differences between HIIE and MIE (P=0.72, ES=0.16). Plasma [triacylglycerol] and [total antioxidant status] were not different between trials. CONCLUSIONS: Exercise intensity plays an important role in protecting the vasculature from the deleterious effects of a HFM. Performing HIIE may provide superior vascular benefits than MIE in adolescent groups

The effects of two weeks high-intensity interval training on fasting glucose, glucose tolerance and insulin resistance in adolescent boys: a pilot study

This is the final version. Available on open access from BMC via the DOI in this recordAvailability of data and materials: The datasets generated and analysed during the current study are not publicly available due to ethical restrictions but are available from the corresponding author upon reasonable request.Background Current evidence of metabolic health benefits of high-intensity interval training (HIIT) are limited to longer training periods or conducted in overweight youth. This study assessed 1) fasting and postprandial insulin and glucose before and after 2 weeks of HIIT in healthy adolescent boys, and 2) the relationship between pre intervention health outcomes and the effects of the HIIT intervention. Methods Seven healthy boys (age:14.3 ± 0.3 y, BMI: 21.6 ± 2.6, 3 participants classified as overweight) completed 6 sessions of HIIT over 2 weeks. Insulin resistance (IR) and blood glucose and insulin responses to a Mixed Meal Tolerance Test (MMTT) were assessed before (PRE), 20 h and 70 h after (POST) the final HIIT session. Results Two weeks of HIIT had no effect on fasting plasma glucose, insulin or IR at 20 h and 70 h POST HIIT, nor insulin and glucose response to MMTT (all P > 0.05). There was a strong negative correlation between PRE training IR and change in IR after HIIT (r = − 0.96, P < 0.05). Conclusion Two weeks of HIIT did not elicit improvements to fasting or postprandial glucose or insulin health outcomes in a group of adolescent boys. However the negative correlation between PRE IR and improvements after HIIT suggest that interventions of this type may be effective in adolescents with raised baseline IR.National Institute for Health Research (NIHR)Northcott Devon Medical Foundatio

High intensity interval exercise is an effective alternative to moderate intensity exercise for improving glucose tolerance and insulin sensitivity in adolescent boys.

JOURNAL ARTICLECopyright © 2014 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.OBJECTIVES: High-intensity interval exercise (HIIE) may offer a time efficient means to improve health outcomes compared to moderate-intensity exercise (MIE). This study examined the acute effect of HIIE compared to a work-matched bout of MIE on glucose tolerance, insulin sensitivity (IS), resting fat oxidation and exercise enjoyment in adolescent boys. DESIGN: Within-measures design with counterbalanced experimental conditions. METHODS: Nine boys (14.2±0.4 years) completed three conditions on separate days in a counterbalanced order: (1) HIIE; (2) work matched MIE, both on a cycle ergometer; and (3) rest (CON). An oral glucose tolerance test (OGTT) was performed after exercise or rest and the area under curve (AUC) responses for plasma [glucose] and [insulin] were calculated, and IS estimated (Cederholm index). Energy expenditure and fat oxidation were measured following the OGTT using indirect calorimetry. Exercise enjoyment was assessed using the Physical Activity Enjoyment Scale. RESULTS: The incremental AUC (iAUC) for plasma [glucose] was reduced following both MIE (-23.9%, P=0.013, effect size [ES]=-0.64) and HIIE (-28.9%, P=0.008, ES=-0.84) compared to CON. The iAUC for plasma [insulin] was lower for HIIE (-24.2%, P=0.021, ES=-0.71) and MIE (-29.1%, P=0.012, ES=-0.79) compared to CON. IS increased by 11.2% after HIIE (P=0.03, ES=0.76) and 8.4% after MIE (P=0.10, ES=0.58). There was a trend for an increase in fat oxidation following HIIE (P=0.097, ES=0.70). Both HIIE and MIE were rated as equally enjoyable (P>0.05, ES<0.01). CONCLUSION: A single bout of time efficient HIIE is an effective alternative to MIE for improving glucose tolerance and IS in adolescent boys immediately after exercise

Involvement of bcl-2 and p21waf1 proteins in response of human breast cancer cell clones to Tomudex

Mechanisms of resistance to Tomudex include increased thymidylate synthase activity, as well as reduced intracellular drug uptake and polyglutamation. However, little is known about other mechanisms of resistance, such as a possible protection against Tomudex-induced apoptosis mediated by bcl-2. We transfected the MDA-MB-435 human breast cancer cell line, which is characterized by a mutated p53 gene, with cDNA of the bcl-2 gene and generated two clones (MDA-bcl4 and MDA-bcl7) characterized by bcl-2 expression twofold and fourfold that observed in the control cell clone (MDAneo). A concomitant overexpression of p21wafl was also detected in the MDA-bcl7 clone. The MDA-bcl4 clone was three times more resistant to a 24-h Tomudex exposure than the MDAneo clone, whereas the MDA-bcl7 clone was as sensitive to Tomudex as the control cell clone. A lower sensitivity of the MDA-bcl4 clone than MDAneo and MDA-bcl7 clones to 5-fluorouracil and gemcitabine was also observed. No significant difference was noted in the susceptibility of clones to fludarabine and methothrexate. Basal levels of thymidylate synthase activity were superimposable in the three clones. Tomudex induced a marked accumulation of cells in the S phase in all the clones. However, an apoptotic hypodiploid DNA peak and the characteristic nuclear morphology of apoptosis were observed only in the MDA-bcl7 clone after exposure to Tomudex. No difference in the treatment-induced modulation of proteins involved in cell cycle progression (cyclin A, cdk2, pRB, E2F-1) and apoptosis (bcl-2, bax) was observed in the three clones. The only exception was that the expression of p21wafl in the MDA-bcl4 clone was inducible at a Tomudex concentration much higher than that required to induce the protein in the other clones. Overall, the results indicate that bcl-2 and p21wafl proteins concur in determining the cellular profile of sensitivity/resistance to Tomudex. © 1999 Cancer Research Campaig

Boron δ-doped (111) diamond solution gate field effect transistors.

A solution gate field effect transistor (SGFET) using an oxidised boron δ-doped channel on (111) diamond is presented for the first time. Employing an optimised plasma chemical vapour deposition (PECVD) recipe to deposit δ-layers, SGFETs show improved current-voltage (I-V) characteristics in comparison to previous similar devices fabricated on (100) and polycrystalline diamond, where the device is shown to operate in the enhancement mode of operation, achieving channel pinch-off and drain-source current saturation within the electrochemical window of diamond. A maximum gain and transconductance of 3 and 200μS/mm are extracted, showing comparable figures of merit to hydrogen-based SGFET. The oxidised device shows a site-binding model pH sensitivity of 36 mV/pH, displaying fast temporal responses. Considering the biocompatibility of diamond towards cells, the device's highly mutable transistor characteristics, pH sensitivity and stability against anodic oxidation common to hydrogen terminated diamond SGFET, oxidised boron δ-doped diamond SGFETs show promise for the recording of action potentials from electrogenic cells

MicroRNA Expression and Clinical Outcome of Small Cell Lung Cancer

The role of microRNAs in small-cell lung carcinoma (SCLC) is largely unknown. miR-34a is known as a p53 regulated tumor suppressor microRNA in many cancer types. However, its therapeutic implication has never been studied in SCLC, a cancer type with frequent dysfunction of p53. We investigated the expression of a panel of 7 microRNAs (miR-21, miR-29b, miR-34a/b/c, miR-155, and let-7a) in 31 SCLC tumors, 14 SCLC cell lines, and 26 NSCLC cell lines. We observed significantly lower miR-21, miR-29b, and miR-34a expression in SCLC cell lines than in NSCLC cell lines. The expression of the 7 microRNAs was unrelated to SCLC patients' clinical characteristics and was neither prognostic in term of overall survival or progression-free survival nor predictive of treatment response. Overexpression or downregulation of miR-34a did not influence SCLC cell viability. The expression of these 7 microRNAs also did not predict in vitro sensitivity to cisplatin or etoposide in SCLC cell lines. Overexpression or downregulation of miR-34a did not influence sensitivity to cisplatin or etoposide in SCLC cell lines. In contrast to downregulation of the miR-34a target genes cMET and Axl by overexpression of miR-34a in NSCLC cell lines, the intrinsic expression of cMET and Axl was low in SCLC cell lines and was not influenced by overexpression of miR-34a. Our results suggest that the expression of the 7 selected microRNAs are not prognostic in SCLC patients, and miR-34a is unrelated to the malignant behavior of SCLC cells and is unlikely to be a therapeutic target

Identification of Genes that Elicit Disuse Muscle Atrophy via the Transcription Factors p50 and Bcl-3

Skeletal muscle atrophy is a debilitating condition associated with weakness, fatigue, and reduced functional capacity. Nuclear factor-kappaB (NF-κB) transcription factors play a critical role in atrophy. Knockout of genes encoding p50 or the NF-κB co-transactivator, Bcl-3, abolish disuse atrophy and thus they are NF-κB factors required for disuse atrophy. We do not know however, the genes targeted by NF-κB that produce the atrophied phenotype. Here we identify the genes required to produce disuse atrophy using gene expression profiling in wild type compared to Nfkb1 (gene encodes p50) and Bcl-3 deficient mice. There were 185 and 240 genes upregulated in wild type mice due to unloading, that were not upregulated in Nfkb1−/− and Bcl-3−/− mice, respectively, and so these genes were considered direct or indirect targets of p50 and Bcl-3. All of the p50 gene targets were contained in the Bcl-3 gene target list. Most genes were involved with protein degradation, signaling, translation, transcription, and transport. To identify direct targets of p50 and Bcl-3 we performed chromatin immunoprecipitation of selected genes previously shown to have roles in atrophy. Trim63 (MuRF1), Fbxo32 (MAFbx), Ubc, Ctsl, Runx1, Tnfrsf12a (Tweak receptor), and Cxcl10 (IP-10) showed increased Bcl-3 binding to κB sites in unloaded muscle and thus were direct targets of Bcl-3. p50 binding to the same sites on these genes either did not change or increased, supporting the idea of p50:Bcl-3 binding complexes. p65 binding to κB sites showed decreased or no binding to these genes with unloading. Fbxo9, Psma6, Psmc4, Psmg4, Foxo3, Ankrd1 (CARP), and Eif4ebp1 did not show changes in p65, p50, or Bcl-3 binding to κB sites, and so were considered indirect targets of p50 and Bcl-3. This work represents the first study to use a global approach to identify genes required to produce the atrophied phenotype with disuse

Meditation on the Soles of the Feet Practice Provides Some Control of Aggression for Individuals with Alzheimer’s Disease

Alzheimer’s disease is a progressive neurodegenerative condition that affects cognition, mental and physical health, and functionality of older people. As the disease progresses from the mild to moderate stage, there is a concomitant increase in several behavioral variables, chiefly agitation, anger, and aggression. Currently, there are no evidence-based treatments for these behaviors in this population. Three individuals with moderate Alzheimer’s disease were taught an informal mindfulness practice, meditation on the Soles of the Feet (SoF), as a self-management strategy within a multiple-baseline design across participants. All three were able to learn and use the SoF practice to manage their verbal and physical aggression. Their use of the SoF practice was correlated with decreased perceived psychological stress for their spouses and caregivers, as well as for the participants, but to a much smaller degree. In terms of social validity, the participants, their spouses, and caregivers rated the SoF practice as acceptable, effective, with no unintended effects, and indicated that they would recommend the practice to others. However, they also rated SoF as effortful for the participants because it involves the participants remembering to use the practice with rising anger, a requirement particularly challenging for those with memory problems. The SoF practice may enable individuals in the early stages of dementia to manage their anger and aggression. The data were derived from an internally valid experimental design, suggestive of initial proof-of-concept, but needs to be replicated before any clinical implications can be imputed from this study