Anthropogenic climate change is a multi-faceted problem. Rising CO₂ levels in the atmosphere cause a warming of global temperatures, acidify the oceans and may ultimately deplete aquatic oxygen, leading to hypoxia. By itself, any one of these conditions can pose a real challenge to an animal, but how the stressors interact is still largely unexplored. Aquatic hypoxia may be especially intricate and, unlike the hypoxic conditions that one might experience when climbing a mountain, is almost always caused by organismal respiration in the water and, thus, is associated with an additional, simultaneous increase in CO₂. The linkage between oxygen and CO₂ levels in water has long been known, but how fish are affected by the combined challenge is poorly studied.

To address the issue, Daniel Montgomery and his colleagues at the University of Exeter, UK, set out to test the effect of rising CO₂ on the hypoxia tolerance of European seabass. They measured the oxygen consumption of the fish while lowering the available oxygen in the water; the point at which the animal can no longer extract oxygen from the depleted water and their oxygen consumption starts to decline is a popular indicator of hypoxia tolerance in fish. Knowing that higher levels of CO₂ tend to acidify the blood of fish – compromising the ability of haemoglobin to bind oxygen and hindering the fish's ability to extract oxygen from the water – Montgomery then supplemented one of the treatments with a simultaneous increase in CO₂, expecting that the combined challenge would render the fish more susceptible to hypoxia.

However, contrary to these predictions, CO₂-treated fish excelled at extracting oxygen from the water and outperformed the low-CO₂ group in terms of hypoxia tolerance. When Montgomery took a closer look at the fish's blood, he found no difference in blood pH between the treatments, indicating a remarkable capacity of the seabass to counteract the acidifying effect of elevated CO₂; surely this is good news for fish that must cope with global rises in CO₂. In addition, fish in the rising CO₂ treatment had a higher haemoglobin–oxygen affinity compared with the low-CO₂ group – a surprising finding, given the common blood pH in the two groups – and this may explain their improved ability to tolerate hypoxia. Haemoglobin is housed within red blood cells, which may actively alter their internal environment to modulate oxygen transport. Whether this is part of the mechanism by which CO₂-exposed seabass increased their haemoglobin–oxygen affinity remains to be seen.

Studying the effects of climate change is complicated as numerous factors may interact to challenge an organism. Understandably, researchers often choose to study single factors in isolation, as this simplifies the interpretation of the data. However, Montgomery and colleagues show that overlooking interaction effects may limit our ability to predict the response of animals to climate change in the wild. In European seabass it appears that the combined condition of a decreasing oxygen level and an increasing CO₂ level in the water, as is found in nature, improves hypoxia tolerance. To account for such effects in future work, current methods to assess hypoxia tolerance in fish should be revised to control for, or at least measure and report, CO₂ levels in the water. Rising CO₂ levels receive a lot of bad press and, in the context of climate change, rightfully so. However, at least for seabass that find themselves gasping for oxygen, the natural rise in CO₂ that comes with aquatic hypoxia may actually save lives.