Decreasing sprint duration from 20 to 10 s during reduced-exertion high-intensity interval training (REHIT) attenuates the increase in maximal aerobic capacity but has no effect on affective and perceptual responses

Purpose: Recent studies have demonstrated that modifying the ‘classic’ 6x30-s ‘all-out’ sprint interval training (SIT) protocol by incorporating either shorter sprints (6x10-s or 15-s sprints) or fewer sprints (e.g. 2x20-s sprints; reduced-exertion high-intensity interval training (REHIT)) does not attenuate the training-induced improvements in maximal aerobic capacity (V̇O2max). The aim of the present study was to determine whether reducing the sprint duration in the REHIT protocol from 20 s to 10 s per sprint influences acute affective responses and the change in V̇O2max following training. Methods: Thirty-six sedentary or recreationally active participants (17 women; mean±SD age: 22±3 y, BMI: 24.5±4.6 kg·m-2, V̇O2max: 37±8 mL·kg-1·min-1) were randomised to a group performing a ‘standard’ REHIT protocol involving 2x20-s sprints or a group who performed 2x10-s sprints. V̇O2max was determined before and after 6 weeks of 3 weekly training sessions. Acute affective responses and perceived exertion were assessed during training. Results: Greater increases in V̇O2max were observed for the group performing 20-s sprints (2.77±0.75 to 3.04±0.75 L·min-1; +10%) compared to the group performing 10-s sprints (2.58±0.57 vs. 2.67±3.04 L·min-1; +4%; group×time interaction effect: p<0.05; d=1.06). Positive affect and the mood state vigour increased post-exercise, while tension, depression and total mood disturbance decreased, and negative affect remained unchanged. Affective responses and perceived exertion were not altered by training and were not different between groups. Conclusion: Reducing sprint duration in the REHIT protocol from 20 s to 10 s attenuates improvements in V̇O2max, and does not result in more positive affective responses or lower perceived exertion

Changes in aerobic capacity and glycaemic control in response to reduced-exertion high-intensity interval training (REHIT) are not different between sedentary men and women

Previously it has been reported that reduced-exertion high-intensity interval training (REHIT; total training time of 3 × 10 min per week) improves maximal aerobic capacity in both sedentary men and women, but improves insulin sensitivity in men only. The aim of the present study was to determine whether there is a true sex difference in response to REHIT, or that these findings can be explained by the large interindividual variability in response inherent to all exercise training. Thirty-five sedentary participants (18 women; mean ± SD age for men and women, respectively: age, 33 ± 9 and 36 ± 9 years; body mass index, 25.1 ± 2.1 and 24.1 ± 3.5 kg·m−2; maximal aerobic capacity, 38.6 ± 8.3 and 31.6 ± 4.6 mL·kg−1·min−1) completed a 6-week REHIT programme consisting of eighteen 10-min unloaded cycling sessions with 1 (first session) or 2 (all other sessions) “all-out” 10–20-s sprints against a resistance of 5% of body mass. Maximal aerobic capacity and oral glucose tolerance test-derived insulin sensitivity were determined before and after training. REHIT was associated with an increase in maximal aerobic capacity (2.54 ± 0.65 vs. 2.78 ± 0.68 L·min−1, main effect of time: p &#60; 0.01), a trend toward reduced plasma insulin area-under-the-curve (AUC; 6.7 ± 4.8 vs. 6.1 ± 4.0 IU·min−1·mL−1, p = 0.096), but no significant change in plasma glucose AUC or the Cederholm index of insulin sensitivity. Substantial interindividual variability in response to REHIT was observed for all variables, but there was no significant effect of sex. In conclusion, REHIT improves the key health marker of aerobic capacity within a minimal total training time-commitment. There is large interindividual variability in responses to REHIT, but sex differences in the responses are not apparent

A NEW EPIDERMAL GROWTH FACTOR RECEPTOR INHIBITOR IN COLON CANCER CELLS

Introduction Members of the Epidermal Growth Factor Receptor (EGFRs) family of receptor tyrosine kinases act as critical mediators of the cellular communication network regulating complex biological processes such as proliferation and differentiation. Since EGFRs signalling is frequently deregulated in several human cancers, interference with EGFR activation and/or intracellular signal transduction pathway represents a promising strategy for the development of novel and selective anticancer therapies. Small molecules inhibitors of EGFR as well as monoclonal antibodies to EGFR are being utilized as anti-cancer therapeutics. In this respect a shikonin-derivative, &#61538;-hydroxyisovalerylshikonin, exerts a strong, non-ATP-competitive inhibition of EGFR kinase activity, suggesting that it may bind to the ligand binding site [1]. As this compound has little potential as drug candidate because of its poor solubility, we have designed and synthesized a library of derivatives in order to obtain active compounds endowed with more \u201cdrug-like\u201d properties. In this study we have tested the anti-tumour activity of FR18, the first compound of this class, by using the HT29 colon adenocarcinoma cell model and by comparing its potency with an anti-EGFR-blocking monoclonal antibody. Materials and Methods HT29 cells were exposed to increasing doses of FR18 or EGFR-blocking antibody and cell cycle distribution was evaluated by flow cytometry. The effects induced on EGFR auto-phosphorylation were tested by means of immunoprecipitation and western blotting, while spectral confocal microscopy was used to investigate EGF-receptor interaction. Results While EGFR-blocking antibody treatment induced growth arrest in G0/G1, FR18 determined an increase of HT29 cells in the G2/M phase and apoptotic cell death. At the receptor level, FR18 determined a remarkable reduction of EGFR activation, associated to the inhibition of the ligand-receptor interaction. In conclusion our data suggest that FR18 selectively induces apoptosis in HT29 cancer cells by interfering with EGFR receptor signalling. Bibliografia 1. Nakaya K. et al., A shikonin derivative, b-hydroxyisovalerylshikonin, is an ATP-non-competitive inhibitor of protein tyrosine kinases. Anticancer Drugs 2003, 14:683-693

La pharmacopée royale galénique et chimique de Moyse Charas

Cette thèse comporte trois parties distinctes : 1) Un aperçu de l'histoire médicale et pharmaceutique au XVIIème siècle. 2) La biographie de Moyse Charas, auteur de la Pharmacopée Royale. 3) Une étude de La Pharmacopée Royale Galénique et Chimique. Le XVIIème siècle a été marqué par de grandes découvertes comme, la circulation du sang par Harvey, la mise au point du microscope, des descriptions médicales de plus en plus précises, l'utilisation du quinquina. Certains médecins, s'attachèrent à ramener les esprits vers la clinique, l'observation et l'expérience. La pharmacopée Royale Galénique et Chimique est un ouvrage didactique, qui reflète les cours assurés par Moyse Charas au Jardin Royal des Plantes de Paris L'étude de la Pharmacopée chimique de Charas nous montre qu'au XVIIème siècle la distillation reste le procédé de prédilection des chimistes et que tout l'art de ces derniers consiste à l'appliquer aux matières les plus diverses, sinon les plus étranges.CHATENAY M.-PARIS 11-BU Pharma. (920192101) / SudocSudocFranceF