Introduction: Age-associated alterations in cardiac structure and function have been observed from the molecular to whole organ level in humans and mammalian models. Understanding the mechanisms involved is important for explaining the development of cardiac disease with age and developing novel strategies for its treatment and prevention. The zebrafish represents a potentially powerful model for ageing studies, as it can model various cardiac pathologies, it is easily genetically modified, and it is a relatively low cost and high-throughput option. In aged zebrafish, myocyte hypertrophy, ventricular density and fibrosis, and valvular lesions, as well as reductions in coronary vasculature have been described. The functional consequences of these structural changes, however, have not been well described. In the current study, we investigated age-related changes in cardiac function in the zebrafish.