High-level, acute exposures to individual polycyclic aromatic hydrocarbons (PAHs) and complex PAH mixtures result in cardiac abnormalities in developing fish embryos. Whereas acute PAH exposures can be developmentally lethal, little is known about the later life consequences of early life, lower level PAH exposures in survivors. A population of PAH-adapted Fundulus heteroclitus from the PAH-contaminated Superfund site, Atlantic Wood Industries, Elizabeth River, Portsmouth, Virginia, United States, is highly resistant to acute PAH cardiac teratogenicity. We sought to determine and characterize long-term swimming performance and cardiac histological alterations of a subteratogenic PAH mixture exposure in both reference killifish and PAH-adapted Atlantic Wood killifish embryos. Killifish from a relatively uncontaminated reference site, King's Creek, Virginia, United States, and Atlantic Wood killifish were treated with dilutions of Elizabeth River sediment extract at 24 h post fertilization (hpf). Two proven subteratogenic dilutions, 0.1 and 1.0% Elizabeth River sediment extract (total PAH 5.04 and 50.4 µg/L, respectively), were used for embryo exposures. Then, at 5-mo post hatching, killifish were subjected to a swim performance test. A separate subset of these individuals was processed for cardiac histological analysis. Unexposed King's Creek killifish significantly outperformed the unexposed Atlantic Wood killifish in swimming performance as measured by Ucrit (i.e., critical swimming speed). However, King's Creek killifish exposed to Elizabeth River sediment extract (both 0.1 and 1.0%) showed significant declines in Ucrit. Histological analysis revealed the presence of blood in the pericardium of King's Creek killifish. Although Atlantic Wood killifish showed baseline performance deficits relative to King's Creek killifish, their pericardial cavities were nearly free of blood and atrial and ventricular alterations. These findings may explain, in part, the diminished swimming performance of King's Creek fish. Environ Toxicol Chem 2017;36:3246-3253. © 2017 SETAC.