It was hypothesised that chronic hypoxia acclimation (preconditioning) would alter the behavioural low-O₂ avoidance strategy of fish as a result of both aerobic and anaerobic physiological adaptations. Avoidance and physiological responses of juvenile snapper (Pagrus auratus) were therefore investigated following a 6 week period of moderate hypoxia exposure (10.2–12.1 kPa PO₂, 21±1°C) and compared with those of normoxic controls (PO₂=20–21 kPa, 21±1°C). The critical oxygen pressure (P_crit) limit of both groups was unchanged at ~7 kPa, as were standard, routine and maximum metabolic rates. However, hypoxia-acclimated fish showed increased tolerances to hypoxia in behavioural choice chambers by avoiding lower PO₂ levels (3.3±0.7 vs 5.3±1.1 kPa) without displaying greater perturbations of lactate or glucose. This behavioural change was associated with unexpected physiological adjustments. For example, a decrease in blood O₂ carrying capacity was observed after hypoxia acclimation. Also unexpected was an increase in whole-blood P₅₀ following acclimation to low O₂, perhaps facilitating Hb–O₂ off-loading to tissues. In addition, cardiac mitochondria measured in situ using permeabilised fibres showed improved O₂ uptake efficiencies. The proportion of the anaerobic enzyme lactate dehydrogenase, at least relative to the aerobic marker enzyme citrate synthase, also increased in heart and skeletal red muscle, indicating enhanced anaerobic potential, or in situ lactate metabolism, in these tissues. Overall, these data suggest that a prioritization of O₂ delivery and O₂ utilisation over O₂ uptake during long-term hypoxia may convey a significant survival benefit to snapper in terms of behavioural low-O₂ tolerance.

The effect of altered oxygen transport potential on behavioural responses to environmental hypoxia was tested experimentally in snapper, Pagrus auratus, treated with a haemolytic agent (phenylhydrazine) or a sham protocol. Standard metabolic rate was not different between anaemic and normocythaemic snapper (Hct=6.7 and 25.7 g dl^-1, respectively), whereas maximum metabolic rate, and hence aerobic scope (AS), was consistently reduced in anaemic groups at all levels of water PO₂ investigated (P<0.01). This reduction of AS conferred a higher critical oxygen limit (P_crit) to anaemic fish (8.6±0.6 kPa) compared with normocythaemic fish (5.3±0.4 kPa), thus demonstrating reduced hypoxic tolerance in anaemic groups. In behavioural choice experiments, the critical avoidance PO₂ in anaemic fish was 6.6±2.5 kPa compared with 2.9±0.5 kPa for controls (P<0.01). Behavioural avoidance was not associated with modulation of swimming speed. Despite differences in physiological and behavioural parameters, both groups avoided low PO₂ just below their P_crit, indicating that avoidance was triggered consistently when AS limits were reached and anaerobic metabolism was unavoidable. This was confirmed by high levels of plasma lactate in both treatments at the point of avoidance. This is the first experimental demonstration of avoidance behaviour being modulated by internal physiological state. From an ecological perspective, fish with disturbed oxygen delivery potential arising from anaemia, pollution or stress are likely to avoid environmental hypoxia at a higher PO₂ than normal fish.

Turbidity as a result of increased suspended sediments in coastal waters is an environmental stress of worldwide concern. Recent research on fish suggests that detrimental changes to gill structure can occur in turbid waters, with speculation that these alterations diminish fitness variables, such as growth and development, by negatively impacting the O₂ uptake capacity (respiration) of fish. Specifically to address this unknown, the impact of turbid water on the gill structure, somatic growth rate and O₂ uptake rates of a juvenile sparid species (Pagrus auratus) was addressed following exposure to five different turbidity treatments (<10, 20, 40, 60 or 80 nephelometric turbidity units) for 30 days. Significant gill structural change was apparent with a progressive increase in turbidity and was quantified as a reduction in lamellar density, as well as an increase in basal hyperplasia, epithelial lifting and increased oxygen diffusion distance across the lamellae. The weight of control fish did not change throughout the experiment, but all fish exposed to turbid waters lost weight, and weight loss increased with nephelometric turbidity units, confirming that long-term turbidity exposure is detrimental to growth productivity. The growth of fish could be impacted in a variety of ways, but the specific hypothesis that structural alteration of the gills impairs O₂ uptake across the gills and limits growth fitness was not supported because there was no measurable difference in the standard metabolic rate, maximal metabolic rate, aerobic metabolic scope or critical oxygen saturation limit of fish measured in clear water after 30 days of exposure. Although impaired O₂ uptake as a result of structurally adjusted gills is unlikely to be the cause of poor fish growth, the exact mechanism by which growth productivity is affected in turbid conditions remains unclear and warrants further investigation.