Breath‐holding and its breakpoint

Abstract

This article reviews the basic properties of breath-holding in humans and the possible causes of the breath at breakpoint. The simplest objective measure of breath-holding is its duration, but even this is highly variable. Breath-holding is a voluntary act, but normal subjects appear unable to breath-hold to unconsciousness. A powerful involuntary mechanism normally overrides voluntary breath-holding and causes the breath that defines the breakpoint. The occurrence of the breakpoint breath does not appear to be caused solely by a mechanism involving lung or chest shrinkage, partial pressures of blood gases or the carotid arterial chemoreceptors. This is despite the well-known properties of breath-hold duration being prolonged by large lung inflations, hyperoxia and hypocapnia and being shortened by the converse manoeuvres and by increased metabolic rate. Breath-holding has, however, two much less well-known but important properties. First, the central respiratory rhythm appears to continue throughout breath-holding. Humans cannot therefore stop their central respiratory rhythm voluntarily. Instead, they merely suppress expression of their central respiratory rhythm and voluntarily 'hold' the chest at a chosen volume, possibly assisted by some tonic diaphragm activity. Second, breath-hold duration is prolonged by bilateral paralysis of the phrenic or vagus nerves. Possibly the contribution to the breakpoint from stimulation of diaphragm muscle chemoreceptors is greater than has previously been considered. At present there is no simple explanation for the breakpoint that encompasses all these properties.

Widespread depolarization during expiration: A source of respiratory drive?

“…Breath holding does not stop the central respiratory rhythm; the rhythm continues and is merely suppressed by voluntarily holding the chest at a chosen volume [77]. In addition, the length of time a person is able to hold their breath is increased by bilateral paralysis of the phrenic or vagus nerve, suggesting that stimulation of peripheral diaphragm muscle chemoreceptors may contribute to the breakpoint of breath holding more than previously thought [77].…”

“…In addition, the length of time a person is able to hold their breath is increased by bilateral paralysis of the phrenic or vagus nerve, suggesting that stimulation of peripheral diaphragm muscle chemoreceptors may contribute to the breakpoint of breath holding more than previously thought [77]. Duration of breath-holding has been shown to be reduced by factors that increase feedback from diaphragm afferents, such as tonic diaphragm activity, or factors that increase the central respiratory rhythm, such as hypoxia or hypercapnia, decreasing lung volume, or increased metabolic rate [77]. During breath-holding, respiratory drive is stimulated when the breaking point is reached, likely due to elevated levels of CO 2 , there is a growing urge to breath and involuntary contractions of respiratory muscles known as involuntary breathing movements (IBMs) [78].…”

A bilateral cortico-bulbar network associated with breath holding in humans, determined by functional magnetic resonance imaging

“…Evidence for whether respiratory rhythmic output persists during breath holding is unclear. In cats, medullary neuronal activity is quiescent during behaviourally conditioned breath holding (Orem and Netick, 1986), whereas recent evidence in humans has shown that sinus arrhythmia, indicative of central respiratory rhythmic output, may persist during volitional breath holding (Parkes, 2006), and in a clinical study of a patient with supranuclear palsy, automatic breathing persisted, albeit reduced, during a volitionally induced breath hold (Haouzi et al, 2006). These latter results suggest that central respiratory rhythmic output cannot be stopped voluntarily but that there is a behavioural influence on central respiratory control and that neuronal output is suppressed either prior to the motoneurones or at the level of the motoneurones in the spinal cord that innervate the respiratory musculature.…”

“…Whilst a voluntary breath hold is easy to initiate, it will eventually be terminated when strong involuntary mechanisms overwhelm the volitional inhibitory control (Godfrey and Campbell, 1968;Parkes, 2006). Numerous physiological factors, e.g., lung volume, blood gas composition and respiratory muscle contraction, that together with non-physiological factors, e.g., anxiety or willpower, determine the length and breaking point of a breath hold, which can be highly variable between individuals and even within the same individual (Godfrey and Campbell, 1968;Parkes, 2006). At present, there is no information on the neural mechanisms that either underlie the voluntary inhibition of spontaneous breathing during a breath hold or determine the breath hold breaking point.…”

Opioids Depress Cortical Centers Responsible for the Volitional Control of Respiration

“…In this study, we investigated the effect of the opioid remifentanil on volitional respiration by assessing changes in the brain centers that mediate a short expiratory breath hold. Breath holding is initially a motor act, but soon causes a strong urge to breathe, which eventually overpowers the volitional inhibitory act (Parkes, 2006). Breath holding therefore tests both the motor and sensory/affective components of respiration.…”