During live export, abalone are transported in air, exposing them to environmental hypoxia for extended periods. Hypoxia-inducible factor-1 (HIF-1), a fundamental moderator of hypoxia, activates a variety of genes in response to hypoxic stress, including inducible nitric oxide synthase (iNOS), which is involved in vasodilation, which ultimately can lead to improved perfusion. This study hypothesized that Haliotis midae, the South African abalone, recruits the under-perfused left gill during hypoxia via HIF-1 and iNOS induction whereas changing metabolic rates, transitions to anaerobic respiration and maintaining circulating oxygen by means of reverse Bohr shift that contribute to alleviating tissue hypoxia during 24-h air exposure. Haliotis midae were exposed to air for 24 h as a proxy for hypoxia and were reimmersed in water for 1 h for recovery before the HIF-1α protein expression, iNOS gene expression and ¹⁴C inulin space were measured in the gills. We also measured oxygen consumption rates, hemolymph D-lactate levels, pH, and PO₂. We found no evidence of HIF-mediated iNOS induction, but abalone hypometabolism and the presence of lactic acid in circulation during the short recovery indicate some reliance on anaerobiosis.