An insulin based model to explain changes and interactions in human breath-holding

Until now oxygen was thought to be the leading factor of hypoxic conditions. Whereas now it appears that insulin is the key regulator of hypoxic conditions. Insulin seems to regulate the redox state of the organism and to determine the breakpoint of human breath-holding. This new hypoxia-insulin hypotheses might have major clinical relevance. Besides the clinical relevance, this hypothesis could explain, for the first time, why the training of the diaphragm, among other factors, results in an increase in breath-holding performance. Elite freedivers/apnea divers are able to reach static breath-holding times to over 6 min. Untrained persons exhibit an unpleasant feeling after more or less a minute. Breath-holding is stopped at the breakpoint. The partial oxygen pressure as well as the carbon dioxide pressure failed to directly influence the breakpoint in earlier studies. The factors that contribute to the breakpoint are still under debate. Under hypoxic conditions the organism needs more glucose, because it changes from the oxygen consuming pentose phosphate (36 ATP/glucose molecule) to the anaerobic glycolytic pathway (2ATP/glucose molecule). Hence insulin, as it promotes the absorption of glucose, is set in the center of interest regarding hypoxic conditions. This paper provides an insulin based model that could explain the changes and interactions in human breath-holding. The correlation between hypoxia and reactive oxygen species (ROS) and their influence on the sympathetic nerve system and hypoxia-inducible factor 1 alpha (HIF-1α) is dealt with. It reviews as well the direct interrelation of HIF-1α and insulin. The depression of insulin secretion through the vagus nerve activation via inspiration is discussed. Furthermore the paper describes the action of insulin on the carotid bodies and the diaphragm and therefore a possible role in respiration pattern. Freedivers that go over the breakpoint of breath-holding could exhibit seizures and thus the effect of insulin, blood glucose levels and corticosteroids in hippocampal seizures is highlighted.