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Aim: Physical activity (PA) is a key component for brain health and Reserve, and it is among the main dementia protective factors. However, the neurobiological mechanisms underpinning Reserve are not fully understood. In this regard, a noradrenergic (NA) theory of cognitive reserve (Robertson, 2013) has proposed that the upregulation of NA system might be a key factor for building reserve and resilience to neurodegeneration because of the neuroprotective role of NA across the brain. PA elicits an enhanced catecholamine response, in particular for NA. By increasing physical commitment, a greater amount of NA is synthetised in response to higher oxygen demand. More physically trained individuals show greater capabilities to carry oxygen resulting in greater Vo2max – a measure of oxygen uptake and physical fitness (PF). Methods: We hypothesized that greater Vo2max would be related to greater Locus Coeruleus (LC) MRI signal intensity. In a sample of 41 healthy subjects, we performed Voxel‐Based Morphometry analyses, then repeated for the other neuromodulators as a control procedure (Serotonin, Dopamine and Acetylcholine). Results: As hypothesized, greater Vo2max related to greater LC signal intensity, and weaker associations emerged for the other neuromodulators. Conclusion: This newly established link between Vo2max and LC–NA system offers further understanding of the neurobiology underpinning Reserve in relationship to PA. While this study supports Robertson's theory proposing the upregulation of the NA system as a possible key factor building Reserve, it also provides ground for increasing LC–NA system resilience to neurodegeneration via Vo2max enhancement. [ABSTRACT FROM AUTHOR]

The ability to detect and correct errors is critical to adaptive control of behaviour and represents a discrete neuropsychological function. A number of studies have highlighted that attention-deficit hyperactivity disorder (ADHD) is associated with abnormalities in behavioural and neural responsiveness to performance errors. One limitation of previous work has been a failure to determine the extent to which these differences are attributable to failures of conscious error awareness, a process that is dependent on the integrity of the frontal lobes. Recent advances in electrophysiological research make it possible to distinguish unconscious and conscious aspects of error processing. This study constitutes an extensive electrophysiological investigation of error awareness and error processing in ADHD. A Go/No-Go response inhibition task specifically designed to assess error awareness was administered to a group of adults diagnosed with ADHD and a group of matched control participants. The ADHD group made significantly more errors than the control group but was less likely to consciously detect these errors. An analysis of event-related potentials elicited by errors indicated that an early performance monitoring component (early positivity) was significantly attenuated in the ADHD group as was a later component that specifically reflects conscious error processing (Pe). Dipole source modelling suggested that abnormal Pe amplitudes were attributable to decreased activation of the anterior cingulate cortex. Decreased electrodermal activity in the ADHD group also suggested a motivational insensitivity to performance errors. Our data provide evidence that neuropsychological deficits associated with ADHD can be exacerbated by error processing abnormalities. Error awareness may represent an important cognitive and physiological phenotype for ADHD. (Contains 6 figures and 3 tables.)

The present study examines a new alertness training strategy (Self-Alert Training, SAT) designed to explore the relationship between the top-down control processes governing arousal and sustained attention. In order to maximally target frontal control systems SAT combines a previously validated behavioural self-alerting technique [Robertson, I. H., Tegner, R., Tham, K., Lo, A., & Nimmo-Smith, I. (1995). "Sustained attention training for unilateral neglect: Theoretical and rehabilitation implications." "Journal of Clinical and Experimental Neuropsychology," 17, 416-430] with an autonomic arousal biofeedback protocol in which participants learn to modulate their own arousal levels. The SAT protocol was first validated with a group of 23 neurologically healthy participants and then independently tested in a group of 18 adults with ADHD to determine its clinical utility. Half of the participants in each group were assigned to a placebo condition to control for non-specific effects. All participants performed the sustained attention to response task (SART) during pre- and post-training testing sessions to assess training effects on sustained attention. By the end of SAT all participants were able to modulate their own arousal levels without external prompting. Comparison of pre- and post-training baseline data indicated that, as predicted, SAT was associated with increased levels of autonomic arousal accompanied by improved accuracy on the SART. In contrast, participants in the placebo condition exhibited a gradual reduction in arousal over time and increased reaction time variability indicative of a vigilance decrement. These data demonstrate that the recruitment of top-down control processes during volitional modulation of arousal leads to improved sustained attention. These findings have important implications for the rehabilitation of attention deficits arising from frontal dysfunction. (Contains 4 tables and 5 figures.)