Hypoxia and hypercapnia often accompany seawater warming and interactively alter marine ectotherm performance, potentially threatening their populations. To detail mechanistic responses, we investigated whole-animal physiology alongside cellular homeostasis in a species expected to be relatively robust to their impacts, the oyster Ostrea edulis. Acute warming alone (W) and combined with hypercapnia and hypoxia (deadly trio, DT) started at 18°C, increasing stepwise by 2°C per 48 hours until critical temperatures (34 °C). Mortality onset at a lower temperature under DT than W but rates equalized by 34°C. DT-exposed oysters’ hemolymph PO2 began 29% lower at 18°C, but by 34°C was only slightly lower than in W oysters. In both groups, resting metabolic rate (RMR) and heart rate rose with warming. Hemolymph PO2 was stable until 26°C, whence it declined. DT elicited a higher heart rate, which began to fall after ∼32°C, while heart rate in W-exposed oysters continued rising. Relative increases in branchial metabolite levels of alanine and fumarate, profiled via 1H-NMR spectroscopy, indicated greater contributions of anaerobic metabolism in DT- than W-exposed oysters. Gill tissue showed higher levels of the mitochondrial stabilizer sirtuin-5 alongside higher antioxidative capacity under DT than W-exposed oysters, before declining at temperatures beyond 30°C. Muscle intracellular pH, gill heat shock protein 70 and metabolic profiles appeared unaffected by DT compared to warming. Our results suggest that DT places an additional energetic burden on the oyster, lowering the critical temperature. Nevertheless, tolerance patterns indicate resilience to DT, which may require a re-balancing of passive tolerance mechanisms, especially a probable emphasis on metabolic depression.
Reddin et al. (Mon,) studied this question.