Arterial chemoreceptors, ventilation and heart rate in man.

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Abstract
1. Transient changes of heart rate (HR) and ventilation were recorded following step changes in alveolar gas composition in three healthy subjects. From a steady state of normo‐ or slightly hypercapnic hypoxia (PA,CO2 38‐46 torr, PA,O2 50‐60 torr) arterial chemoreceptor stimulation was transiently relieved by breathing a CO2‐free mixture for two breaths, either pur O2 (causing a fall in PA,CO2 and a rise in PA,O2; O2 test) or a low O2 mixture (causing a fall in PA,CO2 without any change in PA, O2; CO2 test). For both test types ventilation was either allowed to change freely ('free‐breathing' tests) or was consciously maintained at the pre‐test level by the subjects ('controlled‐breathing tests). The circulatory delay from the lungs to the ear was measured with a sensitive ear oximeter. 2. In all 'free‐breathing' tests ventilation decreased significantly after a mean latency of 5.2 sec; the average lung‐ear circulation time was 4.9 sec. HR increased slightly above pre‐test levels in eighty‐one of one hundred and four tests of all types, the changes being significant after a latency identical to that of the ventilatory changes. Except in the 'controlled‐breathing' CO2 tests this early tachycardia was followed by a decrease in HR within the following 5‐6 sec. 3.These findings indicate that the primary effect of withdrawal of arterial chemoreceptor stimulation in conscious man as in the anesthetized animal is tachycardia. The secondary development of bradycardia in 'free‐breathing' CO2 tests is probably due to the operation of a lung reflex sensing changes in ventilation. The absence of bradycardia in 'controlled‐breathing' CO2 tests and its presence in 'controlled‐breathing' O2 tests, finally, suggest that relief of systemic hypoxia causes a slowing of the heart not due to lung reflexes but to some other mechanism which operates with a latency nearly twice as long as the arterial chemoreflex.