Why Does My Breathing Stop When Falling Asleep?

Brief pauses in breathing at the moment you drift off to sleep are surprisingly common and, in most cases, completely normal. When you transition from wakefulness to sleep, your brain’s automatic breathing controls undergo a kind of reset. A backup system called the “wakefulness drive to breathe” switches off, and your body has to rely entirely on chemical signals in the blood to keep the rhythm going. That handoff doesn’t always go smoothly, and the result can be a few seconds where breathing stalls before it restarts on its own. The sensation can be alarming, but it sits on a spectrum that ranges from a harmless quirk of sleep physiology to a sign of a treatable medical condition.

What the Wakefulness Drive Actually Does

During the day, your breathing is governed by two overlapping systems. One is chemical: sensors in the brain and blood vessels detect carbon dioxide levels and adjust your breathing rate accordingly. The other is a neural stimulus tied to being awake. Simply being conscious provides an extra push to keep air moving in and out. Researchers call this the wakefulness drive, and it acts like a safety net. Even if your carbon dioxide levels dip slightly, the wakefulness drive keeps your diaphragm contracting at a steady pace.

The moment you start falling asleep, that safety net drops away. Carbon dioxide has to rise a little before the chemical sensors pick up the slack and signal the diaphragm to contract again. That brief lag can produce a pause in breathing that lasts anywhere from a few seconds to around 20 seconds. One review of central sleep apnea mechanisms described this as the loss of the “wakefulness drive to breathe,” noting that some rise in blood carbon dioxide is likely at the onset of sleep as a result.1PubMed Central. What is central sleep apnea? Sleep researchers have documented that irregular breathing at sleep onset is common in healthy people and usually considered a normal sleep pattern.2Journal of Korean Sleep Research Society. Sleep-onset Central Sleep Apnea

The Carbon Dioxide Tipping Point

To understand why the pause happens, you need to know about a threshold that only matters when you’re asleep. During wakefulness, your breathing continues even if carbon dioxide in the blood drops relatively low. During sleep, especially the lighter stages of non-REM sleep, a sharp cutoff appears: if carbon dioxide falls below a certain level, breathing stops altogether until the gas builds back up. Researchers call this the apneic threshold, and it is remarkably sensitive. Small, transient dips in blood carbon dioxide pressure below your normal resting level are enough to shut breathing down, and it doesn’t restart until carbon dioxide climbs well above where it was before the pause.3PubMed Central. The ventilatory responsiveness to CO2 below eupnoea as a determinant of ventilatory stability in sleep

This is why the transition into sleep is the most vulnerable window. A few slightly deeper breaths as you relax, maybe a sigh or a shift in position, can push your carbon dioxide below that threshold. Once it drops, your breathing pauses. Carbon dioxide accumulates during the pause, crosses back above the threshold, and breathing starts again. The whole cycle can repeat several times before your sleep deepens and the system stabilizes. Research on the apneic threshold during non-REM sleep has confirmed that even modest changes in ventilatory drive alter how close your resting carbon dioxide sits to the threshold, making some people more prone to pauses than others.4PubMed. Crossing the apnoeic threshold: causes and consequences

Animal studies that systematically lowered carbon dioxide during sleep found that the gap between normal breathing levels and the apneic threshold was only about 5 mmHg. That margin narrowed or widened depending on the type of respiratory stimulus present. Reduced ventilatory drive narrowed the gap and increased susceptibility to apnea, while conditions that boosted drive generally widened it, with one exception: low oxygen levels actually narrowed the gap despite increasing breathing rate.5American Journal of Respiratory and Critical Care Medicine. Effect of Ventilatory Drive on Carbon Dioxide Sensitivity below Eupnea during Sleep That last finding helps explain why certain conditions, like sleeping at high altitude, tend to make breathing pauses worse rather than better.

When the Breathing System Overcorrects

In some people, the pause-restart cycle at sleep onset doesn’t settle down. Instead, it gets stuck in a loop: breathing stops, carbon dioxide rises, the body overreacts with a burst of deep breaths, carbon dioxide drops too low again, and breathing stops once more. Sleep scientists describe this with a concept called loop gain, which is essentially a measure of how aggressively your breathing control system responds to changes in blood gases. If loop gain is high, your system overcorrects every time, and the result is oscillating cycles of breathing too much and then not at all.

A review of central and complex sleep apnea found that in most cases, the cyclic absence of breathing effort is, paradoxically, a consequence of a hypersensitive chemoreflex response. The system overreacts to oppose changes in airflow, leading to overshoot-and-undershoot oscillations. Transitions between sleep and wakefulness raise the controller gain further and add to the instability.6PubMed Central. Pathogenesis of central and complex sleep apnoea This helps explain why the problem is concentrated around the moment of falling asleep, when you’re bouncing between light sleep and brief arousals. Each arousal temporarily restores the wakefulness drive, which triggers a burst of ventilation, drops carbon dioxide, and sets the whole cascade off again.7PubMed. Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea

Once this becomes a self-sustaining pattern, the result is central sleep apnea, a condition where breathing repeatedly pauses not because the airway is blocked (that would be obstructive sleep apnea) but because the brain temporarily stops sending the signal to breathe. The apnea itself triggers further instability: each pause causes a brief arousal, which provokes hyperventilation, which drops carbon dioxide below threshold, which causes another pause.8PubMed Central. Central Sleep Apnea: a Brief Review

Airway Collapse Adds Another Layer

The carbon dioxide story explains central apneas, the kind where the brain simply stops sending the breathing signal. But many people who notice breathing pauses at sleep onset are also experiencing some degree of airway narrowing. The muscles that hold the throat open relax as you fall asleep, and in people with certain anatomical features, like a naturally narrow airway or extra tissue around the throat, the airway can partially or fully collapse. Decreased activity in the pharyngeal dilator muscles during sleep is one of the key factors that triggers upper airway collapse.9American Journal of Respiratory and Critical Care Medicine. Desipramine Increases Genioglossus Activity and Reduces Upper Airway Collapsibility during Non-REM Sleep in Healthy Subjects

In practice, many people experience a mix of both mechanisms. The brain’s chemical controllers waver at sleep onset, the airway narrows as muscles relax, and the two processes feed into each other. This is why the experience of breathing stopping when falling asleep can feel different on different nights or in different sleeping positions. On your back, gravity pulls the tongue and soft tissue backward, narrowing the airway and making collapse more likely. On your side, the airway stays a bit more open and the problem may be milder.

Heart Failure, Opioids, and High Altitude

Several medical conditions and environmental factors push the breathing control system further toward instability, making pauses longer, more frequent, or more likely to disrupt sleep.

Heart failure is one of the most studied triggers. In people with congestive heart failure, fluid congestion and impaired circulation can cause chronic hyperventilation even while awake, holding carbon dioxide at low levels. During sleep, those already-low levels sit dangerously close to the apneic threshold. Research on heart failure patients found that those with low waking carbon dioxide levels were more likely to develop Cheyne-Stokes respiration during sleep, a distinctive pattern of gradually waxing and waning breathing punctuated by central apneas.10PubMed. Pathogenesis of Cheyne-Stokes respiration in patients with congestive heart failure. Relationship to arterial PCO2

Opioid medications are another well-documented cause. These drugs directly suppress the brainstem’s respiratory centers, disrupting the body’s chemical sensitivity to carbon dioxide. One documented case showed that a patient on opioids had severe central sleep apnea that persisted even with standard positive-airway-pressure therapy but was eliminated with adaptive servo-ventilation. After she discontinued opioids, repeat testing showed complete resolution of the central apneas. When she later gained weight while still off opioids, she developed obstructive sleep apnea instead, confirming that the central pauses were specifically opioid-driven.11PubMed Central. Opioids Cause Central and Complex Sleep Apnea in Humans and Reversal With Discontinuation: A Plea for Detoxification.

High altitude produces a similar effect through a different mechanism. Above roughly 3,000 meters, the low oxygen concentration drives the body to breathe harder, which lowers carbon dioxide. At those altitudes, almost all healthy people develop periodic breathing during non-REM sleep, with cycles of deep breathing followed by pauses. The cause is a hypoxia-driven increase in chemoreceptor sensitivity to carbon dioxide changes, amplifying the overshoot-undershoot pattern described earlier.12PubMed Central. Common High Altitudes Illnesses a Primer for Healthcare Provider If you’ve ever noticed breathing pauses while sleeping in the mountains, this is almost certainly what was happening, and it generally resolves as you acclimatize or return to lower elevations.

Waking Up Gasping or Choking

Some people don’t just notice their breathing pause; they jolt awake with a choking or suffocating sensation. This is understandably frightening and often drives people to seek answers. There are a few distinct things that can cause this experience.

The most common is obstructive sleep apnea, where the airway collapses enough to cut off airflow. The brain detects the rising carbon dioxide and falling oxygen and triggers a brief arousal, which often comes with a gasp or a snort as the airway reopens. In central sleep apnea, the arousal can also produce a choking sensation even though the airway was never blocked, because waking up with carbon dioxide elevated and oxygen low feels like suffocating regardless of the mechanism.

Interestingly, research on parasomnias has found that choking sensations during sleep can also arise from arousal disorders unrelated to any breathing problem. A study of sleepwalkers found that about 13% had occasional choking sensations during sleep, and these episodes occurred exclusively during arousals from deep (N3) sleep despite normal airway patency and no epileptic activity. The patients showed intense stress responses during these events. Roughly 38% of patients in a sleep apnea comparison group also reported occasional choking, but in their case the cause was identifiable on standard sleep testing.13Sleep Medicine. Choking during sleep: can it be expression of arousal disorder? The takeaway is that not every choking sensation at sleep onset points to apnea. Anxiety, arousal disorders, and even acid reflux can mimic the experience.

Why Babies Are More Vulnerable

Breathing pauses during sleep aren’t just an adult phenomenon. Infants, especially premature babies, are far more susceptible. The reason traces back to the same carbon dioxide threshold. In newborns, the gap between normal resting carbon dioxide and the level that triggers apnea is dramatically smaller than in adults. One study measured this gap in neonates and found it averaged only about 1.15 Torr, compared with roughly 3.5 Torr in adult subjects. The researchers concluded that this narrow margin makes the infant respiratory control system highly vulnerable, because even minor fluctuations in breathing can push carbon dioxide below threshold and stop breathing altogether.14PubMed. Measurement of the CO2 apneic threshold in newborn infants: possible relevance for periodic breathing and apnea

The breathing pattern itself also differs between infants and adults. In premature infants, periodic breathing tends to follow a crescendo-decrescendo pattern, where breaths gradually build in size and then taper off before a pause. In adults, periodic breathing more often shows a predominantly decrescendo pattern. Despite these differences, the duty cycle, meaning the fraction of each cycle spent actively breathing, remains consistent across ages.15PubMed. The morphology of periodic breathing in infants and adults In healthy full-term infants, periodic breathing at sleep onset is common and typically resolves as the respiratory control system matures over the first several months of life.

Hormones and Sex Differences

Women tend to develop sleep-disordered breathing at lower rates than men during their reproductive years, and hormones appear to play a role. Progesterone is a known respiratory stimulant: it increases the sensitivity of the brain’s carbon dioxide sensors, which effectively widens the gap between normal breathing levels and the apneic threshold. This makes pauses less likely. Research has linked low progesterone levels with increased sleep-disordered breathing.16PubMed Central. Sleep Disturbances Across a Woman’s Lifespan: What Is the Role of Reproductive Hormones?

This protective effect appears to weaken after menopause, when progesterone and estrogen levels decline sharply. The rates of sleep apnea in postmenopausal women begin to approach those seen in men. However, the exact mechanism is still debated. One study that specifically tracked breathing events in women across hormonal changes found that the apnea-hypopnea index didn’t change significantly with sex hormone deficiency, suggesting that other factors tied to aging or body composition may be at least as important as the hormonal shift itself.17PubMed. Sleep, breathing, and menopause: the effect of fluctuating estrogen and progesterone on sleep and breathing in women

What Treatment Looks Like for Persistent Central Apnea

If your breathing pauses are occasional, happen only right at sleep onset, and don’t leave you feeling exhausted or gasping awake, they probably fall within the normal range of sleep-onset breathing variation. But if the pauses are frequent enough to fragment your sleep, leave you with morning headaches, or produce excessive daytime sleepiness, a sleep study can identify whether you have central or obstructive sleep apnea, or a combination of both.

For central sleep apnea specifically, the American Academy of Sleep Medicine issued updated guidelines recommending continuous positive airway pressure (CPAP) as a first-line treatment across most subtypes, including primary central apnea, apnea related to heart failure, and apnea caused by medications or substances. The recommendation is conditional, reflecting low certainty of evidence, but CPAP can stabilize carbon dioxide levels enough to prevent the overshoot-undershoot cycling. For cases where CPAP alone doesn’t resolve the problem, adaptive servo-ventilation (ASV) is suggested as an alternative. ASV devices continuously adjust the pressure and breathing support breath by breath, counteracting the oscillations in real time. The guidelines note that ASV in patients with heart failure and reduced ejection fraction should be used only at experienced centers with close monitoring.18PubMed Central. Treatment of central sleep apnea in adults: an American Academy of Sleep Medicine clinical practice guideline

For opioid-related central apnea, the most effective intervention documented is discontinuation of the opioid itself, which has been shown to resolve the breathing pauses completely in some cases.11PubMed Central. Opioids Cause Central and Complex Sleep Apnea in Humans and Reversal With Discontinuation: A Plea for Detoxification. For altitude-related periodic breathing, descent is the definitive fix, though acetazolamide, a medication that mildly acidifies the blood and stimulates ventilation, is sometimes used as a preventive measure for people sleeping above 3,000 meters.

Sleep Position, Alcohol, and Other Practical Factors

A few things within your control can influence how often breathing pauses at sleep onset. Sleeping on your back places the tongue and soft palate in a position where gravity can narrow the airway, increasing the likelihood of both obstructive and mixed-type apneas. Side sleeping tends to keep the airway more open. Alcohol relaxes the upper airway muscles more than normal sleep does, making collapse more likely, and it also blunts the arousal response that would normally wake you up to resume breathing. The result is that breathing pauses after drinking tend to be longer and more frequent.

Nasal congestion can also play a role by forcing mouth breathing, which changes airway geometry and can increase the negative pressure inside the throat during inhalation. Some people notice their breathing pauses get worse during allergy season or with a cold, and this is part of why. Sleep deprivation is another underappreciated factor. When you’re extremely tired, you fall into deeper sleep more quickly, and the transitions between sleep stages are less gradual. The wakefulness drive drops out more abruptly, and the chemical control system has less time to adjust, creating a window where pauses are more likely.

For people who experience the sensation of breathing stopping only occasionally and without other symptoms, these practical measures may be all that’s needed. But if you consistently wake up feeling unrefreshed, if a bed partner notices long or frequent pauses, or if you find yourself fighting sleepiness during the day, those are signs that what’s happening goes beyond the normal sleep-onset hiccup and warrants a conversation with a sleep specialist.