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Direct assessment of attitudes toward socially sensitive topics can be affected by deception attempts. Reaction-time based indirect measures, such as the Implicit Association Test (IAT), are less susceptible to such biases. Neuroscientific evidence shows that deception can evoke characteristic ERP differences. However, the cerebral processes involved in faking an IAT are still unknown. We randomly assigned 20 university students (15 females, 24.65 +/- 3.50 years of age) to a counterbalanced repeated-measurements design, requesting them to complete a Brief-IAT (BIAT) on attitudes toward doping without deception instruction, and with the instruction to fake positive and negative doping attitudes. Cerebral activity during BIAT completion was assessed using high-density EEG. Event-related potentials during faking revealed enhanced frontal and reduced occipital negativity, starting around 150 ms after stimulus presentation. Further, a decrease in the P300 and LPP components was observed. Source analyses showed enhanced activity in the right inferior frontal gyrus between 150 and 200 ms during faking, thought to reflect the suppression of automatic responses. Further, more activity was found for faking in the bilateral middle occipital gyri and the bilateral temporoparietal junction. Results indicate that faking reaction-time based tests alter brain processes from early stages of processing and reveal the cortical sources of the effects. Analyzing the EEG helps to uncover response patterns in indirect attitude tests and broadens our understanding of the neural processes involved in such faking. This knowledge might be useful for uncovering faking in socially sensitive contexts, where attitudes are likely to be concealed.
Introduction
We investigated blood glucose (BG) and hormone response to aerobic high-intensity interval exercise (HIIE) and moderate continuous exercise (CON) matched for mean load and duration in type 1 diabetes mellitus (T1DM).
Material and Methods
Seven trained male subjects with T1DM performed a maximal incremental exercise test and HIIE and CON at 3 different mean intensities below (A) and above (B) the first lactate turn point and below the second lactate turn point (C) on a cycle ergometer. Subjects were adjusted to ultra-long-acting insulin Degludec (Tresiba/ Novo Nordisk, Denmark). Before exercise, standardized meals were administered, and short-acting insulin dose was reduced by 25% (A), 50% (B), and 75% (C) dependent on mean exercise intensity. During exercise, BG, adrenaline, noradrenaline, dopamine, cortisol, glucagon, and insulin-like growth factor-1, blood lactate, heart rate, and gas exchange variables were measured. For 24 h after exercise, interstitial glucose was measured by continuous glucose monitoring system.
Results
BG decrease during HIIE was significantly smaller for B (p = 0.024) and tended to be smaller for A and C compared to CON. No differences were found for post-exercise interstitial glucose, acute hormone response, and carbohydrate utilization between HIIE and CON for A, B, and C. In HIIE, blood lactate for A (p = 0.006) and B (p = 0.004) and respiratory exchange ratio for A (p = 0.003) and B (p = 0.003) were significantly higher compared to CON but not for C.
Conclusion
Hypoglycemia did not occur during or after HIIE and CON when using ultra-long-acting insulin and applying our methodological approach for exercise prescription. HIIE led to a smaller BG decrease compared to CON, although both exercises modes were matched for mean load and duration, even despite markedly higher peak workloads applied in HIIE. Therefore, HIIE and CON could be safely performed in T1DM.