COVID-19 National Football League (NFL) Injury Analysis: Follow-Up Study.

Background: In 2020, COVID-19 spread across the world and brought normal daily life to a halt, causing the shutdown of nearly everything in order to prevent its spread. The National Football League (NFL) similarly experienced shutdowns and the resulting effects, leaving athletes unable to train in some of the most advanced facilities with many of the best trainers in the world. A previous study, titled COVID-19 Return to Sport: NFL Injury Prevalence Analysis, determined that there was increased injury prevalence during the 2020 season, likely due to decreased physiological adaptations within athletes' bodies as a result of facility shutdowns.

COVID-19 Return to Sport: NFL Injury Prevalence Analysis.

Background: Sport injuries have been common among athletes across the globe for decades and have the potential to disrupt athletic careers, performance, and psyche. Many health professionals and organizations have undertaken injury mitigation strategies to prevent sport injuries through protective equipment, training protocols, and a host of other evidence-based practices. Many of these specialized training methods were disrupted due to protocols to mitigate the spread of COVID-19.

Bethanechol and N-acetylcysteine mimic feeding signals and reverse insulin resistance in fasted and sucrose-induced diabetic rats.

Meal-induced insulin sensitization (MIS) is explained by the HISS (hepatic insulin sensitizing substance) hypothesis. In the presence of two "feeding signals," a pulse of insulin results in the release of HISS from the liver. HISS acts selectively on skeletal muscle and doubles the response to insulin.

Acetylcholinesterase antagonist potentiated insulin action in fed but not fasted state.

The glucose disposal effect of insulin is doubled in response to a meal. This meal-induced insulin sensitization results from insulin acting on the liver, in the presence of a permissive hepatic parasympathetic feeding signal and elevated hepatic glutathione (GSH), to release hepatic insulin-sensitizing substance (HISS), a hormone that acts selectively on skeletal muscle to stimulate insulin-mediated glucose uptake. Blockade of the parasympathetic feeding signal to the liver, either through surgical denervation or atropine-mediated antagonism of hepatic muscarinic receptors, eliminates the HISS response, resulting in HISS-dependent insulin resistance (HDIR) and decreasing the response to insulin by approximately 55% in the fed state.

Meal-induced insulin sensitization in conscious and anaesthetized rat models comparing liquid mixed meal with glucose and sucrose.

We have recently shown that meal-induced insulin sensitization (MIS) occurs after feeding and decreases progressively to insignificance after 24 h of fasting and is caused by action of a hepatic insulin sensitizing substance (HISS). In order to carry out quantitative studies of MIS, some standardized meal intake is required. Our objective was to establish animal models to be tested in both the conscious and anaesthetized state using intragastric injection of liquid meals in order to quantify MIS.