METHODS: Participants (N = 16; 8 boys; age 12.5 ± 0.8 years) performed, on separate days, HIIE cycling consisting of 8 × 1-min work-intervals at 100%-to-70% (HIIEH-L), 70%-to-100% (HIIEL-H) or 85% (HIIECON) peak power separated by 75 s recovery. Affect, enjoyment and cerebral haemodynamics (oxygenation (∆O2Hb), deoxygenation (∆HHb) and tissue oxygenation index (TOI)) were recorded before, during, and after all conditions.
RESULTS: Affect and enjoyment were lower during HIIEH-L compared to HIIEL-H and HIIECON at work-intervals 1 to 3 (all P 0.83) but were greater during HIIEH-L than HIIEL-H and HIIECON at work-interval 8 (all P 0.83). ∆O2Hb was similar across conditions (P = 0.87) but TOI and ∆HHb were significantly greater and lower, respectively during HIIEH-L compared to HIIEL-H and HIIECON at work-interval 8 (all P 0.40). Affect was correlated with TOI (all r > 0.92) and ∆HHb (all r > -0.73) across conditions.
CONCLUSIONS: HIIEH-L offers advancement to the HIIECON and HIIEL-H which bring significant greater affect and enjoyment towards the end HIIE work-interval, implicating the feasibility and adoption of this protocol for health promotion in youth. Also, changes in prefrontal cortex haemodynamics are associated with the affect during HIIE.
METHODS: RPE, heart rate (HR), and oxygen uptake (V˙O2) data were retrospectively extracted from 3 lab-based crossover studies, with a pooled sample size of 45 adolescents, performing either cycling-based or running-based HIIE sessions. Within-participant correlations were calculated for RPE-HR and RPE-V˙O2, and receiver operator characteristic curve analysis was used to establish RPE cut points.
RESULTS: The results showed that RPE-HR demonstrated acceptable criterion validity (r = .53-.74, P < .01), while RPE-V˙O2 had poor validity (r = .40-.48, P < .01), except for HIIE at 100% peak power (r = .59, P < .01). RPE cut points of 4 and 5 were established in corresponding to HR/V˙O2 based thresholds.
CONCLUSION: RPE has some utility in evaluating intensity during lab-based running or cycling HIIE in adolescents. Future studies should expand the validation and calibration of RPE for prescribing and monitoring HIIE in children and adolescents in field-based contexts.
METHODS: Diabetes was induced by intraperitoneal (i.p.) injection of streptozotocin (55 mg/kg) in to male Sprague-Dawley rats. Rats were divided into six different groups; normal control rats were not induced with STZ and served as reference, STZ diabetic control rats were given normal saline. Three groups were treated with OS aqueous extract at 0.2, 0.3 and 0.5 g/kg, orally twice daily continuously for 21 d. The fifth group was treated with glibenclamide (6 mg/kg) in aqueous solution orally continuously for 21 d. After completion of the treatment period, biochemical parameters and expression levels of glucose transporter 2 (Slc2a2), glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PCK1) were determined in liver by quantitative real time PCR.
RESULTS: Administration of OS at different doses to STZ induced diabetic rats, resulted in significant decrease (P<0.05) in blood glucose level in a dose dependent manner by 36%, 48%, and 64% at doses of 0.2, 0.3 and 0.5 g/kg, respectively, in comparison to the STZ control values. Treatment with OS elicited an increase in the expression level of Slc2a2 gene but reduced the expression of G6Pase and PCK1 genes. Morefore, OS treated rats, showed significantly lower levels of serum alanine transaminase (ALT), aspartate aminotransferase (AST) and urea levels compared to STZ untreated rats. The extract at different doses elicited signs of recovery in body weight gain when compared to STZ diabetic controls although food and water consumption were significantly lower in treated groups compared to STZ diabetic control group.
CONCLUSIONS: O. sumatrana aqueous extract is beneficial for improvement of hyperglycemia by increasing gene expression of liver Slc2a2 and reducing expression of G6Pase and PCK1 genes in streptozotocin-induced diabetic rats.
MATERIALS AND METHODS: In silico target prediction was first employed to predict the probability of the polyphenols interacting with key protein targets related to insulin signalling, based on a model trained on known bioactivity data and chemical similarity considerations. Next, CA was investigated in in vivo studies where induced type 2 diabetic rats were treated with CA for 28 days and the expression levels of genes regulating insulin signalling pathway, glucose transporters of hepatic (GLUT2) and muscular (GLUT4) tissue, insulin receptor substrate (IRS), phosphorylated insulin receptor (AKT), gluconeogenesis (G6PC and PCK-1), along with inflammatory mediators genes (NF-κB, IL-6, IFN-γ and TNF-α) and peroxisome proliferators-activated receptor gamma (PPAR-γ) were determined by qPCR.
RESULTS: In silico analysis shows that several of the top 20 enriched targets predicted for the constituents of CA are involved in insulin signalling pathways e.g. PTPN1, PCK-α, AKT2, PI3K-γ. Some of the predictions were supported by scientific literature such as the prediction of PI3K for epigallocatechin gallate. Based on the in silico and in vivo findings, we hypothesized that CA may enhance glucose uptake and glucose transporter expressions via the IRS signalling pathway. This is based on AKT2 and PI3K-γ being listed in the top 20 enriched targets. In vivo analysis shows significant increase in the expression of IRS, AKT, GLUT2 and GLUT4. CA may also affect the PPAR-γ signalling pathway. This is based on the CA-treated groups showing significant activation of PPAR-γ in the liver compared to control. PPAR-γ was predicted by the in silico target prediction with high normalisation rate although it was not in the top 20 most enriched targets. CA may also be involved in the gluconeogenesis and glycogenolysis in the liver based on the downregulation of G6PC and PCK-1 genes seen in CA-treated groups. In addition, CA-treated groups also showed decreased cholesterol, triglyceride, glucose, CRP and Hb1Ac levels, and increased insulin and C-peptide levels. These findings demonstrate the insulin secretagogue and sensitizer effect of CA.
CONCLUSION: Based on both an in silico and in vivo analysis, we propose here that CA mediates glucose/lipid metabolism via the PI3K signalling pathway, and influence AKT thereby causing insulin secretion and insulin sensitivity in peripheral tissues. CA enhances glucose uptake and expression of glucose transporters in particular via the upregulation of GLUT2 and GLUT4. Thus, based on its ability to modulate immunometabolic pathways, CA appears as an attractive long term therapy for T2DM even at relatively low doses.