Early life stages of salmonids are particularly vulnerable to warming and hypoxia, which are common stressors in hyporheic, gravel bed, rearing habitat (i.e. a 'redd'). With the progression of global climate change, high temperatures and hypoxia may co-occur more frequently within redds, particularly for salmonid species at their southern range limit. Warming and hypoxia have competing effects on energy supply and demand, which can be detrimental to energy-limited early life stages. We examined how elevated temperature and hypoxia as individual and combined stressors affected the survival, physiological performance, growth, and development of Chinook salmon (Oncorhynchus tshawytscha). We reared late fall-run Chinook salmon from fertilization to the fry stage in a fully factorial design of two temperatures [10°C (ambient) and 14°C (warm)] and two oxygen levels [normoxia (100% air saturation, 10 mg O2/l) and hypoxia (50% saturation, 5.5 mg O2/l)]. Rearing in hypoxia significantly reduced hatching success, especially in combination with warming. Both warming and hypoxia improved acute thermal tolerance. While rearing in hypoxia improved tolerance to acute hypoxia stress, warming reduced hypoxia tolerance. Hypoxia-reared fish were smaller at hatch, but were able to reach similar sizes to the normoxia-reared fish by the fry stage. High temperature and normoxia resulted in the fastest rate of development while low temperature and hypoxia resulted in the slowest rate of development. Despite improved physiological tolerance to acute heat and hypoxia stress, hypoxia-reared embryos had reduced survival and growth, which could have larger population-level effects. These results suggest that both warming and hypoxia are important factors to address in conservation strategies for Chinook salmon.

A warming climate poses a fundamental problem for embryos that develop within eggs because their demand for oxygen (O2) increases much more rapidly with temperature than their capacity for supply, which is constrained by diffusion across the egg surface. Thus, as temperatures rise, eggs may experience O2 limitation due to an imbalance between O2 supply and demand. Here, we formulate a mathematical model of O2 limitation and experimentally test whether this mechanism underlies the upper thermal tolerance in large aquatic eggs. Using Chinook salmon (Oncorhynchus tshawytscha) as a model system, we show that the thermal tolerance of eggs varies systematically with features of the organism and environment. Importantly, this variation can be precisely predicted by the degree to which these features shift the balance between O2 supply and demand. Equipped with this mechanistic understanding, we predict and experimentally confirm that the thermal tolerance of these embryos in their natural habitat is substantially lower than expected from laboratory experiments performed under normoxia. More broadly, our biophysical model of O2 limitation provides a mechanistic explanation for the elevated thermal sensitivity of fish embryos relative to other life stages, global patterns in egg size and the extreme fecundity of large teleosts.

Warming and hypoxia are two stressors commonly found within natural salmon redds that are likely to co-occur. Warming and hypoxia can interact physiologically, but their combined effects during fish development remain poorly studied, particularly stage-specific effects and potential carry-over effects. To test the impacts of warm water temperature and hypoxia as individual and combined developmental stressors, late fall-run Chinook salmon embryos were reared in 10 treatments from fertilization through hatching with two temperatures [10°C (ambient) and 14°C (warm)], two dissolved oxygen saturation levels [normoxia (100% air saturation, 10.4-11.4 mg O₂/l) and hypoxia (50% saturation, 5.5 mg O₂/l)] and three exposure times (early [eyed stage], late [silver-eyed stage] and chronic [fertilization through hatching]). After hatching, all treatments were transferred to control conditions (10°C and 100% air saturation) through the fry stage. To study stage-specific effects of stressor exposure we measured routine metabolic rate (RMR) at two embryonic stages, hatching success and growth. To evaluate carry-over effects, where conditions during one life stage influence performance in a later stage, RMR of all treatments was measured in control conditions at two post-hatch stages and acute stress tolerance was measured at the fry stage. We found evidence of stage-specific effects of both stressors during exposure and carry-over effects on physiological performance. Both individual stressors affected RMR, growth and developmental rate while multiple stressors late in development reduced hatching success. RMR post-hatch showed persistent effects of embryonic stressor exposure that may underlie differences observed in developmental timing and acute stress tolerance. The responses to stressors that varied by stage during development suggest that stage-specific management efforts could support salmon embryo survival. The persistent carry-over effects also indicate that considering sub-lethal effects of developmental stressor exposure may be important to understanding how climate change influences the performance of salmon across life stages.