LAUSR

Acute exposure to low oxygen (hypoxia) places conflicting demands on the heart. Whilst an increase in heart rate (tachycardia) may compensate systemic oxygen delivery as arterial oxygenation falls, the heart itself is an energetically expensive organ that may benefit from slowing (bradycardia) to reduce work when oxygen is limited. Both strategies are apparent in vertebrates, with tetrapods (mammals, birds, reptiles, and amphibians) classically exhibiting hypoxic tachycardia and fishes displaying characteristic hypoxic bradycardia. With a richer understanding of the ontogeny and evolution of the responses, however, we see similarities in the underlying mechanisms between vertebrate groups. For example, in adult mammals, primary bradycardia results from the hypoxic stimulation of carotid body chemoreceptors that are overwhelmed by mechano‐sensory feedback from the lung associated with hyperpnoea. Fish‐like bradycardia prevails in the mammalian foetus (which, at this stage, is incapable of pulmonary ventilation), and in fish and foetus alike, the bradycardia ensues despite an elevation of circulating catecholamines. In both cases, the reduced heart rate may primarily serve to protect the heart. Thus, the comparative perspective offers fundamental insight into how and why different vertebrates regulate heart rate in different ways during periods of hypoxia.