Severe hypoxemia during apnea in humans : influence of cardiovascular responses

Abstract

When a diving human holds his or her breath, the heart beat slows and the blood vessels constrict in large portions of the body. In diving mammals such as seals, similar responses effectively conserve oxygen for the brain, enabling them to dive very deep and to stay underwater for a long time.

The principal aim of this thesis was to study the biological significance of bradycardia (a slowing of the heart rate) and vasoconstriction during apnea in exercising humans. The question was whether these cardiovascular mechanisms also in humans would temporarily "conserve" oxygen (i.e. temporarily reduce 02 uptake in muscles etc.) and thus protect the brain from a level of hypoxia that would otherwise cause unconsciousness in a breath-hold diver.

A second aim was to determine the inter-individual variation among the human subjects in terms of the degree of bradycardia during apnea, in order to explore whether the intensity of these cardiovascular responses would make some individuals more fit to survive underwater swimming and apnea than others.

Our results indeed showed inter-individual differences such that a high degree of bradycardia during apnea correlated significantly with higher levels (= better conservation) of arterial oxygen saturation. Thus, the subjects with the lowest heart rates during exercise and apnea had the best preserved saturation measured with earlobe pulse oximetry. Also, we found that the cardiovascular responses to apnea in exercising humans clearly delay the development of hypoxemia by reducing the rate of uptake from the main oxygen store, i.e. the lungs.

We found that stroke volume of the heart was not altered during apnea with air and consequently that the bradycardia was associated with a proportional reduction of the cardiac output. There was a significant correlation between the degree of vasoconstriction and the intensity of the bradycardia in the group of subjects, so that subjects with the largest degree of vasoconstriction also had the largest degree of bradycardia. We also found that when the breath was held with oxygen and there was no hypoxemia, stroke volume was increased and the increase in blood pressure was delayed but reached the same high level as during apnea when hypoxemia developed due to lack of oxygen.

We measured heart rates during static apnea (the ability to hold your breath as long as possible without passing out) in both training and competition. We found that heart rates were significantly higher both before and during competitive apnea than the corresponding control values during training. One of our subjects experienced a hypoxia-induced loss of motor control during the competition. We suggest that there is an increased risk of hypoxic syncope due to the reduced bradycardia during competitive apnea, compared to training.

We also report results from experiments on breath-hold diving to 40 in depth, and underwater swimming in a pool, supporting the notion that the heart rate responses to apnea observed under the present laboratory conditions fairly well represent those occurring during actual breath-hold diving.