OK, here's what I've got:
1. Alkalosis = left shift of oxygen dissociation curve, reducing tissue oxygen delivery and favouring anaerobic respiration = higher lactate.
2. Alkalosis activates glycolytic enzymes (including PFK) = more pyruvate than Kreb can handle = higher lactate https://twitter.com/MattyR86/status/1359222423191769091
https://doi.org/10.1097/00003246-199109000-00005
8 patients in ICU given lactate infusions during period of normo- and hypo-ventilation. During hypoventilation, baseline lactate was 60% higher (inversely proportional to CO2). Post infusion, lactate elimination 1/2 life increased 118% in hypovented period
Their discussion claims intracellular pH is major determinant of hepatic lactate metabolism, with optimal range 7.05-7.30. Outside this range, liver releases rather than extracts lactate from circulation.
https://doi.org/10.1093/ndt/gfn585
This group saw 34 patients with panic disorder in A&E, and demonstrated correlation between CO2 (and thus pH) and lactate: The lower the CO2, the higher the lactate
In discussion, they suggest the compensatory mechanisms for respiratory alkalosis reliant on renal handling of bicarbonate are too slow (24-48 hours) and therefore acute alternatives must occur; including organic acid production (hello lactate!)
This is in response to a great thread from @wheezylikesund1

Clearly it's complicated beyond my full understanding, can anyone else shed further light?
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