Holding your breath, known as apnea, triggers complex physiological responses that affect heart rate in contradictory ways. Whether the heart rate increases or decreases depends heavily on the context, such as whether the action occurs in air or involves water immersion. While the body’s initial reaction to a lack of breathing often leans toward an increased heart rate, a separate, powerful reflex frequently overrides this tendency, especially during submersion. The net change in heart rate results from a balance between these competing autonomic nervous system signals.
Immediate Physiological Response to Apnea
When breathing stops, gas exchange ceases, immediately changing blood chemistry. Carbon dioxide (\(\text{CO}_2\)) levels begin to rise, and oxygen (\(\text{O}_2\)) levels start to fall. Chemoreceptors in the carotid arteries and aorta are sensitive to the increase in \(\text{CO}_2\), which is the body’s primary signal to breathe.
The rising \(\text{CO}_2\) stimulates the sympathetic nervous system, responsible for the “fight or flight” response. This activation attempts to increase heart rate (tachycardia) and blood pressure to deliver more blood to tissues, even though no fresh oxygen is available. This default response to respiratory distress often causes the initial heart rate increase noticed at the beginning of a breath-hold. However, this sympathetic drive is quickly challenged or overridden by a specialized, oxygen-conserving reflex.
The Dominant Influence of the Mammalian Dive Reflex
The most significant physiological change during prolonged apnea, especially when combined with facial contact with water, is the activation of the Mammalian Dive Reflex (MDR). This reflex is an innate, multi-system response present in all vertebrates, designed to conserve oxygen for the heart and the brain. The trigger for this reflex is the stimulation of sensory receptors, particularly those supplied by the trigeminal nerve in the face, by cold water.
Once activated, the MDR initiates a slowing of the heart rate, known as bradycardia, mediated by the parasympathetic nervous system through the vagus nerve. This reduction decreases the heart’s workload and its oxygen consumption. Simultaneously, the sympathetic nervous system causes peripheral vasoconstriction, restricting blood flow to the limbs, skin, and abdominal organs. This shunting mechanism redirects the remaining oxygen-rich blood toward the core, ensuring the brain and heart receive preferential perfusion.
Situational Variables That Alter the Heart Rate
The specific heart rate response during breath-holding is not fixed and varies widely based on several external and internal conditions. Water temperature is a significant factor; colder water dramatically enhances the dive reflex, resulting in a more pronounced drop in heart rate. Conversely, breath-holding in warm air or water still causes mild bradycardia, but the effect is less intense because the facial cold receptors are not strongly stimulated.
The body’s starting state also influences the response. Breath-holding after strenuous exercise, which results in high initial \(\text{CO}_2\) and a high baseline heart rate, may see the heart rate remain elevated or even increase further due to conflicting demands. Intentional hyperventilation before a breath-hold artificially lowers the initial \(\text{CO}_2\) level, delaying the uncomfortable urge to breathe.
This delay suppresses the early sympathetic drive but allows the \(\text{O}_2\) level to drop dangerously low before the body signals distress. Psychological state can temporarily interfere with the reflex. High anxiety or stress increases sympathetic nervous system activity, which may momentarily counteract the parasympathetic slowing effect of the dive reflex. This can lead to an initial increase in heart rate, even during submersion, until the parasympathetic drive fully exerts its dominance.
Understanding the Limits of Breath-Holding
Pushing the limits of breath-holding carries a significant risk due to the body’s specialized mechanisms for regulating respiration. The primary urge to breathe is triggered by rising \(\text{CO}_2\), not falling \(\text{O}_2\). When \(\text{CO}_2\) levels are artificially lowered through hyperventilation, the body’s natural alarm system is disabled.
This suppression of the breathing urge allows the oxygen level in the blood to fall below the threshold required to sustain consciousness, leading to a hypoxic blackout. This loss of consciousness, often called shallow water blackout, can occur without warning, even in shallow water. It poses a fatal drowning risk, especially when practiced alone.