Notwithstanding, no study to date has examined the effect of uncoated ATP disodium supplementation on cognitive performance following high-intensity exercise. Thus, inadequate availability of metabolic resources may lead to acute or long-term cognitive impairments (9) and correspondingly, interventions that sustain ATP levels may have application for attenuating cognitive dysfunction in the face of an acute stressor that challenges brain energy metabolism. Cerebral activity is coupled to ATP metabolism, where energy flux is tightly correlated with energy demand (8). Acute deficits in cognitive performance have also been reported in both young adults (6) and children (7) following high-intensity exercise. Consistent with this, when oral ATP was administered in the form of non-coated ATP disodium, beneficial effects including reduced fatigue (3), improved strength, power, and body composition (5), and enhanced recovery (6) were observed. However, a recent study demonstrated that ingestion of 400mg uncoated ATP disodium for 15 days prevented decreases in ATP, adenosine diphosphate (ADP), and adenosine monophosphate (AMP) in the bloodstream for up to 30 minutes following high-intensity exercise when compared to placebo (3). Initial studies providing oral enteric coated ATP disodium displayed no apparent efficacy toward enhancing ATP levels, and subsequent research questioned the bioavailability of enteric coated ATP following oral administration (1,2). Oral ATP disodium (adenosine 5'- triphosphate disodium) is a commercially available product available alone and as a constituent in a number of sports supplements that is purported to maintain ATP levels during high-intensity exercise.
Acute deficits in cognitive performance have also been reported in both young adults and children following high-intensity exercise however, the effects of supplemental ATP on cognitive performance has not been studied.
Our observations indicate that realistic complex mixtures of environmental pollutants can affect neuronal connectivity via NGF-induced neurite outgrowth.Oral ATP disodium (adenosine 5'- triphosphate disodium) is a commercially available product available alone and as a constituent in a number of sports supplements that is purported to maintain ATP levels and improve performance during high-intensity exercise. Neither the POP mixture nor PFOS affected neurite length in the absence of NGF. PFOS induced neurite outgrowth to about 50 % of the level seen with the POP mixture. The pollutants did not inhibit neuritogenesis, but rather increased NGF-induced neurite length. Live imaging, using the IncuCyte ZOOM platform indicated ongoing cell proliferation over time, but slower in presence of NGF. Robust glutathione levels were observed in NGF-differentiated cells. High-content analysis showed a decrease in cell number, but no changes for nuclear and mitochondrial cellular health parameters. Only higher concentrations of POP mixture reduced tetrazolium salt (MTT) conversion. We also evaluated perfluorooctane sulfonic acid (PFOS) alone, the most abundant compound in the POP mixture.
Cells were exposed for 72 h to a defined mixture of POPs with chemical composition and concentrations based on blood levels in the Scandinavian population. We investigated their effect on neurite outgrowth in PC12 rat pheochromocytoma cells, in absence or presence of nerve growth factor (NGF), an inducer of neuronal differentiation. Persistent organic pollutants (POPs) are potential developmental neurotoxicants. Disruption of neurite outgrowth is a marker for neurotoxicity.