Effects of different types of verbal encouragement on ankle force and muscle activity

The aim of this study is to investigate (i) the effect of live and recorded verbal encouragement on muscle activity and ankle force; (ii) the effect of communication/extroversion on the variables; (iii) the reliability intra and inter examiners of the variables. Twenty healthy-youngers were assessed by surface electromyography of tibialis anterior and ankle flexion force by an ergometer twice, with one week apart. No difference was found between ankle force (p = 0.373) and root mean square values (RMS) (p = 0.207) for any of the conditions assessed on day 1 nor between examiners 1 and 2 for both live and recorded conditions in RMS (p = 0.207) and force (p = 0.373). Between the 1st and 7th days, there were no differences for any of the conditions on RMS (main effect “Day” p = 0.261, “condition” p = 0.568, interaction p = 0.936) or force (main effect“Day” p = 0.889, “condition” p = 0.781, interaction p = 0.961). Intraclass correlation coefficients (ICCs) for the ankle force were, for without verbal encouragement (ICC2, k = 0.880), live verbal encouragement of examiner 1 (ICC2, k = 0.870), and recorded verbal encouragement of examiner 1 (ICC2, k = 0.920). RMS without verbal encouragement condition (ICC2, k = 0.860), live verbal encouragement of examiner 1 (ICC2, k = 0.930) and recorded verbal encouragement of examiner 1 (ICC2, k = 0.920). Reproducibility between the two examiner’s live encouragements for ankle force (ICC3, k = 0.981) and RMS (ICC3, k = 0.920). There was no effect of the presence or type of the augmented feedback in RMS and ankle force. We conclude that verbal encouragement does not influence ankle torque or muscle activity and there is good to excellent intra and inter rater reliability for subjects’ performance regardless of verbal encouragement modality. In addition, we observed that psychological traits Communication and Emotional stability does not affect the subjects’ strength performance at the ankle

Caffeine Consumption Prevents Diabetes-Induced Memory Impairment and Synaptotoxicity in the Hippocampus of NONcZNO10/LTJ Mice

Diabetic conditions are associated with modified brain function, namely with cognitive deficits, through largely undetermined processes. More than understanding the underlying mechanism, it is important to devise novel strategies to alleviate diabetes-induced cognitive deficits. Caffeine (a mixed antagonist of adenosine A1 and A2A receptors) emerges as a promising candidate since caffeine consumption reduces the risk of diabetes and effectively prevents memory deficits caused by different noxious stimuli. Thus, we took advantage of a novel animal model of type 2 diabetes to investigate the behavioural, neurochemical and morphological modifications present in the hippocampus and tested if caffeine consumption might prevent these changes. We used a model closely mimicking the human type 2 diabetes condition, NONcNZO10/LtJ mice, which become diabetic at 7–11 months when kept under an 11% fat diet. Caffeine (1 g/l) was applied in the drinking water from 7 months onwards. Diabetic mice displayed a decreased spontaneous alternation in the Y-maze accompanied by a decreased density of nerve terminal markers (synaptophysin, SNAP25), mainly glutamatergic (vesicular glutamate transporters), and increased astrogliosis (GFAP immunoreactivity) compared to their wild type littermates kept under the same diet. Furthermore, diabetic mice displayed up-regulated A2A receptors and down-regulated A1 receptors in the hippocampus. Caffeine consumption restored memory performance and abrogated the diabetes-induced loss of nerve terminals and astrogliosis. These results provide the first evidence that type 2 diabetic mice display a loss of nerve terminal markers and astrogliosis, which is associated with memory impairment; furthermore, caffeine consumption prevents synaptic dysfunction and astrogliosis as well as memory impairment in type 2 diabetes