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In my respiratory physiology lectures, my professor explained that hypoxia-induced hyperventilation occurs in 2 stages when people try to acclimate at high altitudes. My question is about the long-term 2nd stage, listed as #2 below:

  1. there's an immediate increase in alveolar ventilation triggered by peripheral chemoreceptors, but this only leads to a small increase, and also decreases levels of $p_{CO_2}$.
  2. over 8 hrs, there's a slow rise and 2 mechanisms are involved:
    a) bicarbonate ion ($HCO_3^-$) in cerebrospinal fluid is shuttled out and chemoreceptors increase their sensitivity to $p_{O_2}$
    b) kidneys excrete more $HCO_3^-$ to normalize blood pH

I get that the $HCO_3^-$ and $H^+$ comes from $H_2CO_3$ being broken down through carbonic anhydrase. But she never mentioned where the $HCO_3^-$ is shuttled to or which chemoreceptors are increasing their sensitivity to $p_{O_2}$ (I assume peripheral since it's mentioning sensitivity to $O_2$). She then says that because of this $H^+$ and $CO_2$ levels increase, stimulating central chemoreceptors to increase ventilation to help decrease the acidity/$CO_2$ levels. I don't understand how $H^+$ and $CO_2$ levels are even rising because I don't know where the $HCO_3^-$ is even going and what it's role is. This professor is terrible at explaining things, and I'm just so confused at this point! Any sort of direction would be so helpful! Thanks!

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not a complete answer, just a comment: $CO_2 + H_2O$ <--> $H_2CO_3$. This is going on all the time (e.g. in a soda bottle) without the need for an enzyme. –  Michael Kuhn Feb 7 '13 at 14:52

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