The Magnitude of Diving Bradycardia During Apnea at Low-Altitude Reveals Tolerance to High Altitude Hypoxia

Abstract

Acute mountain sickness (AMS) is a potentially life-threatening illness that may develop during exposure to hypoxia at high altitude (HA). Susceptibility to AMS is highly individual, and the ability to predict it is limited. Apneic diving also induces hypoxia, and we aimed to investigate whether protective physiological responses, i.e., the cardiovascular diving response and spleen contraction, induced during apnea at low-altitude could predict individual susceptibility to AMS. Eighteen participants (eight females) performed three static apneas in air, the first at a fixed limit of 60 s (A1) and two of maximal duration (A2-A3), spaced by 2 min, while SaO₂, heart rate (HR) and spleen volume were measured continuously. Tests were conducted in Kathmandu (1470 m) before a 14 day trek to mount Everest Base Camp (5360 m). During the trek, participants reported AMS symptoms daily using the Lake Louise Questionnaire (LLQ). The apnea-induced HR-reduction (diving bradycardia) was negatively correlated with the accumulated LLQ score in A1 (r _s = -0.628, p = 0.005) and A3 (r _s = -0.488, p = 0.040) and positively correlated with SaO₂ at 4410 m (A1: r = 0.655, p = 0.003; A2: r = 0.471, p = 0.049; A3: r = 0.635, p = 0.005). Baseline spleen volume correlated negatively with LLQ score (r _s = -0.479, p = 0.044), but no correlation was found between apnea-induced spleen volume reduction with LLQ score (r _s = 0.350, p = 0.155). The association between the diving bradycardia and spleen size with AMS symptoms suggests links between physiological responses to HA and apnea. Measuring individual responses to apnea at sea-level could provide means to predict AMS susceptibility prior to ascent.

Keywords: acute mountain sickness; breath-hold diving; cardiovascular diving response; hypoxia; prediction; spleen.

FIGURE 1

Timing of apneas (A1: apnea 1; A2: apnea 2; A3: apnea 3) with spleen measure (doted line), continuous measure of SaO2 (arterial oxygen saturation, black line) and HR (heart rate, gray line) and lung volume measures. 15 s of hyperventilation preceded apnea 3 (A3) combined with a MVV (maximal voluntary ventilation) test.

FIGURE 2

Sleeping altitudes for data collection of Lake Louise Questionnaire (LLQ) score (days 1–7) included in the analysis during ascent to EBC (n = 18).

FIGURE 3

Recording of an individual participants diving bradycardia during 1 min apnea. Note the initial tachycardia, followed by a decline phase. The diving response was defined as the percentage reduction in HR (heart rate) during the period from 30 s into the apnea until the end of the apnea, marked as Mean HR, which was compared to the period 90–30 s before the apnea (baseline).

FIGURE 4

The figures depict correlation plots of accumulated LLQ score at 4410 m and magnitude of the HR (heart rate) reduction (diving bradycardia) during Apnea 1 (A), Apnea 2 (B) and Apnea 3 (C). (D) Shows HR-reduction (diving bradycardia) during Apnea 1 and SaO₂ at 4410 m.

FIGURE 5

The spleen volume change after three apneic episodes (apnea 1–3) spaced by 2 min of recovery and the volume after 5 min recovery. ^∗∗ indicates p < 0.01 from baseline.

FIGURE 6

Shows a correlation plot between accumulated LLQ score at 4400 m and baseline (resting) spleen volume (A) and maximal volume reduction induced by apnea (B) in Kathmandu at 1400 m.

FIGURE 7

Shows the magnitude of the heart rate (HR) reduction (diving bradycardia) (A) and resting spleen volume (B) for each of the groups based on accumulated acute mountain sickness (AMS) symptoms score: Low LLQ score, Medium LLQ score, and High LLQ score (^∗p < 0.05).

FIGURE 8

Shows correlation plots of accumulated LLQ score at 4400 m and arterial O₂ desaturation during apnea 1 (A), vital capacity (VC; B), and arterial O₂ saturation (SaO₂) at 4400 m (C).