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

Her er et nytt stikk i siden for «oksygen Illusjonen».

I denne studien viser de hvordan «the breakpoint», altså det punktet hvor man ikke greier å holde pusten lenger, ikke har noen assosiasjon med oksygen. Det har assosiasjon med insulin!

Når vi holder pusten og oksygennivået synker, begynner kroppen etterhver å skape energi av sukker. Da økes insulinbehovet. Etter en stund brukes insulinet opp, og først da (!!!) trenger kroppen å puste inn får å få energi fra oksygen igjen.

Oksygen har veldig lite med saken (cellerespirasjon) å gjøre annet enn som en lett tilgjengelig og utømmelig energikilde. Det er interessant å legge merke til at diabetikere, som har lite insulin, har også svært vanskelig for å holde pusten.

Forfatterene beskriver også hvordan trening av diafragma gir evnen til å holde pusten lenger. Og de forklarer hvilke nevrologiske problemer man kan få av å ignorere kroppens signaler om å puste inn, slik konkurransedykkere gjør.

De nevner at vagus nerven reduserer insulin utskillelse. På innpust aktiveres vagus´ afferente (opp til hjernen) signaler pga strekk-reseptorer i lungene, som skrur av innpust-delen av hjernen slik at utpust kan starte (Hering-Breuer reflex). I innpust er det ikke behov for insulin fordi det er nok oksygen tilgjengelig. Derfor gir innpust en stimuli som reduserer insulinutskillelse. Men når man er i innpust-modus i lang tid og opplever hypoxi, vil oksidativt stress virke som et insulin-økende signal. Insulin stimulerer carotid-receptorene, som videre stimulerer hjernen til å aktivere innpust.

Insulin, sammen med kortikosteroider (stresshormoner), stimulerer også intracellulær opphopning av kalsium, som igjen bidrar til nevrologiske problemer.

De nevner også, interessant nok, hvorfor MSM har effekt på prestasjon hos idrettsutøvere.

http://www.ncbi.nlm.nih.gov/pubmed/25801485

Abstract

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 6min. 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 (36ATP/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.

It is accepted that under hypoxic condi- tions the brain switches from the oxygen consuming pentose phos- phate to the glycolytic pathway [21]. Furthermore it has been shown that depending on the paradigm used and brain regions during activation under normoxia, the nonoxidative metabolism increases more than the oxidative one [22]. This strengthens the role of glucose as a major fuel for the brain. Insulin has been shown to reduce hippocampal injury after ischemia [23]. Therefore insulin is a potential key regulator in hypoxic conditions when considering these facts.

The effect of ROS on the musculature is a dose dependent influence on the mus- cle force. In low concentration it increases the muscle force, at high levels it decreases it [28,29] (Fig. 1; Arrow 6, 7). Therefore the redox state of the muscle could be a regulation tool of the isometric muscle force [30]. A possible explanation is that increased ROS pro- duction can alter the calcium release from the sarcoplasmic reticu- lum and also the calcium sensitivity of myofilaments [28,30].

It has been shown that antioxidants can prevent muscular fatigue [31]. The ROS-scavenger N-acetylcysteine [32], as a supporter for glu- tathione resynthesis, postpones the muscle fatigue of an in situ prepared diaphragm [31]. These findings are in line with the reports of elite freedivers that antioxidants like vitamin E, C, resveratrol, methylsulfonylmethane, NAC, coenzyme Q10 etc. have a positive effect on their (static) performance.

During inspiration there should normally be no lack of oxygen and therefore no need for extra insulin. But if there were a lack of oxygen, the organism needs an escape mechanism. This could be accomplished by the previously described rise of ROS, and therefore, via HIF1-a, an increase in the insulin level.

In hypoxic conditions, it appears as insulin secretion rises with increased HIF-a levels.

Insulin triggers the carotid bodies, which should result in diaphragmatic movements.

During breath-holding, insulin secretion is decreased through the activated afferent vagus nerve via the pulmonary stretch receptors. As long as the diaphragm can be hold contracted the stretch receptors are triggered and therefore the insulin secretion is diminished. Hence explaining why training of breath-holding, or better the training of the dia- phragm, results in increased breath-holding performances.

So it seems that insulin is more or less a key regulator in hypoxic conditions. It has to be taken into consideration that under hypoxic situations the organism has to switch to anaerobic meta- bolism and therefore is in need of more glucose. Hence insulin is put into the spotlight of interest when it comes to metabolism under hypoxic conditions and a relative maintenance of a survival fitting redox state

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