Background: The impact of prolonged digital device exposure on physical and mental health in children has been widely investigated by the scientific community. Additionally, the lockdown periods due to the COVID-19 pandemic further exposed children to screen time for e-learning activities. The aim of this systematic review (PROSPERO Registration: CRD42022315596) was to evaluate the effect of digital device exposure on children’s health. The impact of the COVID-19 pandemic was additionally explored to verify the further exposure of children due to the e-learning environment. Methods: Available online databases (PubMed, Google Scholar, Semantic Scholar, BASE, Scopus, Web of Science, and SPORTDiscus) were searched for study selection. The PICO model was followed by including a target population of children aged 2 to 12 years, exposed or not to any type of digital devices, while evaluating changes in both physical and mental health outcomes. The quality assessment was conducted by using the Joanna Briggs Institute (JBI) Critical Appraisal Tool. Synthesis without meta-analysis (SWiM) guidelines were followed to provide data synthesis. Results: Forty studies with a total sample of 75,540 children were included in this systematic review. The study design was mainly cross-sectional (n = 28) and of moderate quality (n = 33). Overall, the quality score was reduced due to recall, selection, and detection biases; blinding procedures influenced the quality score of controlled trials, and outcome validity reduced the quality score of cohort studies. Digital device exposure affected physical activity engagement and adiposity parameters; sleep and behavioral problems emerged in children overexposed to digital devices. Ocular conditions were also reported and associated with higher screen exposure. Home confinement during COVID-19 further increased digital device exposure with additional negative effects. Conclusions: The prolonged use of digital devices has a significant negative impact on children aged 2 to 12, leading to decreased physical activity, sleep disturbances, behavioral issues, lower academic performance, socioemotional challenges, and eye strain, particularly following extended online learning during lockdowns.

Preserving the hydration status means to balance daily fluids and salt losses with gains, where the losses depend on several physiological and environmental factors. Especially for athletes, these losses could be relevant and negatively influence the performance: therefore, their hydro-saline status must be preserved with personalized pre- and rehydration plans all along the performance period. Scientific literature in this field is mainly dedicated to artificial sport drinks. Different territories in most world areas are rich in drinking natural mineral spring waters with saline compositions that reflect their geological origin and that are used for human health (often under medical prescription). However, scarce scientific attention has been dedicated to the use of these waters for athletes. We therefore reviewed the existing literature from the innovative viewpoint of matching spring water mineral compositions with different athletic performances and their hydro-saline requirements.

Reactive oxygen species (ROS) are currently recognized as a key driver of several physiological processes. Increasing evidence indicates that ROS levels can affect myogenic differentiation, but the molecular mechanisms still need to be elucidated. Protein kinase C (PKC) epsilon (PKCe) promotes muscle stem cell differentiation and regeneration of skeletal muscle after injury. PKCs play a tissue-specific role in redox biology, with specific isoforms being both a target of ROS and an up-stream regulator of ROS production. Therefore, we hypothesized that PKCe represents a molecular link between redox homeostasis and myogenic differentiation. We used an in vitro model of a mouse myoblast cell line (C2C12) to study the PKC–redox axis. We demonstrated that the transition from a myoblast to myotube is typified by increased PKCe protein content and decreased ROS. Intriguingly, the expression of the antioxidant enzyme superoxide dismutase 2 (SOD2) is significantly higher in the late phases of myogenic differentiation, mimicking PKCe protein content. Furthermore, we demonstrated that PKCe inhibition increases ROS and reduces SOD2 protein content while SOD2 silencing did not affect PKCe protein content, suggesting that the kinase could be an up-stream regulator of SOD2. To support this hypothesis, we found that in C2C12 cells, PKCe interacts with Nrf2, whose activation induces SOD2 transcription. Overall, our results indicate that PKCe is capable of activating the antioxidant signaling preventing ROS accumulation in a myotube, eventually promoting myogenic differentiation.