Abstract
Bradycardia during submersion has long been known to occur in diving animals.1,2This diving reflex is initiated through a complex cardiovascular reflex partly through cold water stimulation of afferent nerve endings on the body and partly by apnea.3,4Apnea alone causes similar but much less extreme cardiovascular response. The efferent limb of the reflex is mediated through increased sympathetic stimulation of peripheral vasculature (except in heart and brain), which causes vasoconstriction and intense vagal stimulation of the heart. This reflex mechanism prominently seen in aquatic animals allows them to slow their heart rate, decrease oxygen demand, increase oxygen extraction, redistribute blood flow, and maintain arterial pressure when submerged.5Though in a less intense form, man has retained this reflex. Bradycardia is commonly observed in human divers when they are submerged in water.6This reflex is attenuated by a reduction in water temperature7,8and can be
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