Cardio-Respiratory Responses to Breath Hold During Immersion and Submersion in Cold Water: The Role of Exercise and Prior Hyperventilation

Abstract

Loss of consciousness and sudden cardiac death upon submersion is not well understood. Two explanations have been proposed: Shallow water blackout (SWB), also known as hypoxic blackout, and Autonomic Conflict (AC). The proposed mechanism of SWB is hypoxia as a result of hyperventilation abolishing the respiratory drive prior to submersion. AC being described as co-activation of the parasympathetic and sympathetic limbs of the autonomic nervous system (ANS) resulting in fatal cardiac arrhythmias. The four experiments described in this thesis examined the cardio-respiratory responses, including evoked cardiac arrhythmias, to immersion and submersion with breath hold (BH), and the role of hyperventilation and exercise. All studies used a within participant repeated measures design. There are three overarching hypotheses:
1.AC is a more plausible mechanism for loss of consciousness following sudden immersion and submersion compared to SWB following submaximal BHs, with or without moderate hyperventilation.
2.Arrhythmias generated during AC require a sudden change in the magnitude of one limb of the ANS following co-activation of the ANS.
3.Simple reproducible tests that replicate these autonomic loads can predict those at risk of AC.

The first experiment was an empirical study to establish whether SWB or AC was more likely to be responsible for loss of consciousness by examining the effect that prior hyperventilation had on BH time and the cardiac response prior to, and immediately after, the break of BH. In addition, the influence of combining breath holding with immersion or submersion (TW 25 °C), with and without exercise were examined. The results demonstrated that to produce a hypoxic state in the circumstances tested requires the absence of exercise, and prior hyperventilation (EtCO2 3%). There were no episodes of SpO2 less than 90% in any other test conditions; exercise being protective of in this setting. Arrhythmias associated with AC were observed, notable at the break of BH (autonomic disruption), and increased in frequency with hyperventilation, exercise or the combination of the two during submersions.
The aim of the second experiment was to examine the cardio-respiratory response surrounding the break of BH when the magnitude of the autonomic load is increased, by reducing the water temperature to evoke the cold shock response (CSR) with the associated involuntary hyperventilation, using a fixed breath hold time (BHT). The results confirmed that the majority of arrhythmias occurred within 15s of the break of BH; in normoxic and normocapnic conditions; following submersion rather than immersion; but have minimal increase in number between tepid and cold water conditions suggesting either parasympathetic nervous system (PNS) dominance or that a larger change or sudden change in autonomic load is required.
The aim of experiment three was to examine the influence of the PNS on the cardio-respiratory responses, specifically AC, by altering the parasympathetic stimulus via three water temperatures sprayed onto the face to evoke the diving response (DR) on a background of fixed sympathetic load. The results demonstrated an increasing number of arrhythmias with increasing parasympathetic stimulus, but with an apparent plateau suggesting a non-linear relationship. They also showed a small association between the presence of arrhythmia or variability in the RR interval in baseline tests of facial immersion (FI) with concurrent cold pressor test (CPT), and arrhythmias generated during submersions.
In the final experiment, the aim was to determine whether simple tests could reliably predict those at risk of AC during whole body cold water submersions (participants wore immersion suits for cold water submersions (TW 12 °C)), and whether AC was reproducible within susceptible participants. The results demonstrated that ventricular arrhythmias evoked during facial immersion, with concurrent cold pressor test and BH, in participants with a VO2max < 4.00 L.min-1 predicted those who would evoke ventricular arrhythmias during cold water submersions. With repeated submersions the ECG pattern was reproducible but there was a decrease in frequency.
In summary, the findings reported in this thesis demonstrate that:
-AC is a very probable cause of loss of consciousness following sudden submersion in cold water, including when there is a less than maximal lung volume breath hold or absence of changes in hydrostatic pressure exerted on the body.
-When there is supplementary co-activation of the PNS and SNS that a rapid change in one limb of the ANS can evoke arrhythmias.
-Hyperventilation, exercise and increasing autonomic stimulus increased the frequency and severity of arrhythmias, the most severe of which can be predicted from simple tests. Further work is required to establish the sensitivity of predictive tests.

Date of Award	14 Apr 2026
Original language	English
Awarding Institution	University of Portsmouth
Supervisor	Mike Tipton (Supervisor) & Heather Massey (Supervisor)