Oxygen is one of the critical determinants of appropriate embryonic and fetal development, including cardiogenesis. When the demand of tissues for oxygen exceeds oxygen supply, hypoxic conditions develop. In the developing embryo, hypoxia is associated with increased fetal mortality, cerebrovascular anomalies, cardiovascular dysfunction, and altered angiogenesis. Tissue hypoxia may elicit a broad range of responses, many of which are dependent upon hypoxia-inducible transcription factors. Three genes that are stimulated by hypoxia-hypoxia-inducing factor subunit alpha-1, heme oxygenase, hypoxia upregulated protein 1, and cardiac troponin T, which is responsible for binding tropomyosin to regulate calcium binding and contractility of heart muscle-were examined in the embryonic heart of the chicken to determine if expression patterns were altered throughout development. On embryonic day (E) 7, all 3 hypoxic-induced genes were expressed at their highest levels, followed by a decrease from E7 to E19 followed by an increase between internal (E19) and external pipping (E20). The cardiac troponin T exhibited a similar expression level for E7 and E15 with a similar significant increase at E19 and E20. During these periods of development, significant changes in the primary gas exchange organs occur. Based on our observation of upregulation of these hypoxia response genes, it appears that tissue hypoxia is likely a normal component of embryonic development in the chicken based on the upregulation of hypoxia response genes.