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Environmental stressors, such as warm temperatures and hypoxia, can interact and pose a threat to aquatic species. Cross talk between the hypoxia and heat stress cellular pathways can lead to enhanced cross tolerance between these environmental stressors. In this study, we questioned whether elevated temperatures (from 27 degrees to 32 degrees C) during rearing would enhance the hypoxia-inducible transcription factor-1 (HIF-1)-mediated transcriptional response to hypoxia (5% dissolved O-2) in early stages of zebrafish development and whether these differences would be associated with enhanced larval tolerance and survival to hypoxia. We found that embryos reared at 32 degrees C had an enhanced cellular HIF-1 response (elevated hif-1ab and insulin-like growth factor binding-protein mRNA level) and that acute hypoxia (4 h) activated the heat-shock response (elevated hsp70a and hsp90aa mRNA levels). Elevated rearing temperatures and hypoxia exposure also induced precocious hatching, but neither environmental stressor had an effect on the hypoxia tolerance (critical O-2 tension) of 4-d-old larvae and did not protect larvae against the lethal effects of a second acute hypoxia exposure. Overall, during early zebrafish development, cross talk between the hypoxia and heat stress cellular pathways at the gene expression level did not confer cross tolerance at the whole-animal level with respect to hypoxia stress.