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Wim Hof - new cold record

Discussion in 'Cold Thermogenesis' started by smart cat, Jan 5, 2015.

  1. smart cat

    smart cat New Member

    Wim Hof Cheating Death, a documentary

    rlee314 and Kristi Lambert like this.
  2. Jack Kruse

    Jack Kruse Administrator

    brother from another mother
    Kristi Lambert likes this.
  3. Josh

    Josh Gold

    What would limit the maintenance of heart and neural function in the mitochondria during hypothermia? Would all of the ubiquinol be used up as an antioxidant leaving a deficit for starting up the electron transport chain? Would an ubiquinol deficit result in decreased uncoupling and IR production? Or would the generation of reactive Nitrogen and Oxygen species with the failure to recycle Glutathione result in a sudden increase in apoptosis as the ubiquinol antioxodant stores become exhausted?


    Figure 2: Modulation of apoptosis by hypothermia. After a serious insult the cell can trigger apoptosis, a highly regulated cell death mechanism.Intrinsic Pathway. Hypothermia increases ATP stores and slows ion channels then maintaining the integrity of the membranes. Hypothermia applied together or immediately after injury decreases the production of ROS. These events limit the rupture of the outer mitochondrial membrane and the release of proapoptotic molecules like cytochrome c into the cytosol. The hypothermia-induced increase in nitric oxide also avoids cytochrome c release and it is even reported that early NO production can exert a negative feedback regulation of iNOS [34]. Moreover, iNOS transcription activated by NFB was diminished after hypothermia [35]. Since catalase is absent in mitochondria, maintaining GSH redox cycle is critical to avoid H2O2 accumulation. There is abundant evidence that hypothermia keeps GSH pool. Extrinsic Pathway. It was found that hypothermia decreases the affinity of the death ligands-death receptors, with the consequent inhibition of the initiator caspases like caspase-8 or the NFB-family molecules.


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