Influence of hypercapnia and hypercapnic hypoxia on the heart rate response to apnea
Authors: Benjamin R. O'Croinin, Desmond A. Young, Lauren E. Maier, Sean van Diepen, Trevor A. Day, Craig D. Steinback
DOI / Source: 10.14814/phy2.16054
Date: 30 April 2024
Reading level: Intermediate
Why This Matters for Freedivers
Freedivers often assume that “high CO₂” is what drives the strongest diving reflex and the biggest heart-rate drop. This study suggests something more specific: during apneas, it’s mainly low oxygen (hypoxia) that boosts the bradycardia, while extra CO₂ by itself doesn’t add much. That matters for training and safety because it changes what you should blame (and manage) when heart rate drops hard, symptoms feel intense, or rhythm glitches show up—especially near the end of a breath-hold when oxygen is falling.
Synopsis
When you hold your breath, your body flips into oxygen-saving mode: heart rate tends to slow (bradycardia) and blood vessels in the limbs tighten. In freediving, we talk a lot about CO₂ tolerance, and it’s easy to assume that higher CO₂ automatically means a stronger diving response. But oxygen levels also change during breath-holds, and oxygen is the “non-negotiable” fuel for the brain and heart. This paper asks a clean question: which one actually drives the heart-rate drop during apnea—high CO₂, low O₂, or both together?
The researchers tested 26 healthy participants in a controlled lab setup. Instead of letting breathing changes “wash out” the gases, they used a system that precisely controlled end-tidal oxygen and CO₂. Each person performed several short end-expiratory apneas after different pre-breathing conditions: - Normoxia / normal CO₂ (baseline condition), - Hypercapnia (CO₂ raised), - Hypoxia (O₂ lowered), - Hypercapnic hypoxia (CO₂ raised + O₂ lowered together).
Then they compared how much the heart rate fell during the breath-hold under each condition.
Here’s the key result: apneas performed after hypoxia produced a bigger bradycardia than normal conditions. But apneas performed after hypercapnia alone did not significantly increase bradycardia compared to normal. And when they combined hypercapnia + hypoxia, the bradycardia was not bigger than hypoxia alone. In plain terms: oxygen is the main dial for the heart-rate drop during apnea; CO₂ doesn’t seem to turn that dial up by itself.
They also looked at rhythm disturbances (arrhythmias). There wasn’t a clear “statistically proven” increase between conditions, but the combined hypercapnic-hypoxic condition showed the highest count of minor rhythm events, which fits the idea that “stacking stressors” can make the heart’s electrical system a bit more twitchy in some people.
A practical nuance: CO₂ absolutely mattered for urge to breathe—the combined condition shortened apnea time the most. So CO₂ is still very relevant to discomfort and breaking point, but this study suggests it’s not the main driver of the heart-rate slowing during the apnea itself.
For freedivers, the takeaway is a useful mental model: - CO₂ mostly pushes the need to breathe and can increase anxiety/panic sensations. - Low O₂ is what strongly boosts the cardiac diving response (bigger bradycardia) and is also the real safety limiter near the end of the dive.
Abstract
We aimed to determine the relative contribution of hypercapnia and hypoxia to the bradycardic response to apneas. We hypothesized that apneas with hypercapnia would cause greater bradycardia than normoxia, similar to the response seen with hypoxia, and that apneas with hypercapnic hypoxia would induce greater bradycardia than hypoxia or hypercapnia alone. Twenty-six healthy participants (12 females; 23±2 years; BMI 24±3kg/m2) underwent three gas challenges: hypercapnia (+5 torr end tidal partial pressure of CO2 [PETCO2]), hypoxia (50 torr end tidal partial pressure of O2 [PETO2]), and hypercapnic hypoxia (combined hypercapnia and hypoxia), with each condition interspersed with normocapnic normoxia. Heart rate and rhythm, blood pressure, PETCO2, PETO2, and oxygen saturation were measured continuously. Hypercapnic hypoxic apneas induced larger bradycardia (−19±16bpm) than normocapnic normoxic apneas (−11±15bpm; p=0.002), but had a comparable response to hypoxic (−19±15bpm; p=0.999) and hypercapnic apneas (−14±14bpm; p=0.059). Hypercapnic apneas were not different from normocapnic normoxic apneas (p=0.134). After removal of the normocapnic normoxic heart rate response, the change in heart rate during hypercapnic hypoxia (−11±16bpm) was similar to the summed change during hypercapnia+hypoxia (−9±10bpm; p=0.485). Only hypoxia contributed to this bradycardic response. Under apneic conditions, the cardiac response is driven by hypoxia.