Cardiovascular Plasticity and Adaptation of High-Altitude Birds and Mammals.

Exposure to a hypoxic environment at high altitudes imposes severe pressure on animals living there, which utilize substantial cardiovascular and respiratory responses to meet the physiological challenge of oxygen requirement. These responses may result from phenotypic plasticity through short-term exposure (i.e., within a generation) to a new environment or shaped by adaptation (i.e., many generations) through long-term evolution. For example, plasticity triggers a sympathetic-mediated adrenergic response, resulting in an elevation of heart rate and hypoxia-induced pulmonary vasoconstriction that eventually contributes to pulmonary hypertension in some animals. Adaptation to high altitudes can drive an increase in muscular capillarization and adaptive cardiac growth, which promote oxygen diffusion and transportation. Exposure to a high-altitude hypoxic environment stimulates excessive erythropoiesis, which has maladaptive effects and contributes to chronic mountain sickness. Maladaptation caused by plasticity at early stages can be reversed during adaptation. Despite extensive research on high-altitude adaptation, the phenotypic changes and genetic variations in cardiovascular systems responding to high-altitude hypoxia remain insufficiently integrated across taxa. While genomic and transcriptomic studies have advanced our understanding, a cross-taxa comparison of cardiovascular adaptations is still incomplete. We here review recent literature on phenotypic plasticity, adaptations, and genetic and transcriptional basis of cardiovascular systems of mammals and birds living in high altitudes with respect to their duration of exposure at high altitudes. By integrating and comparing data across mammalian and avian species, we aim to provide a framework for understanding the plasticity and adaptation of the cardiovascular system in high-altitude environments.