Respiratory neuromuscular output during breath holding

Abstract

The involuntary respiratory muscle contractions that occur during breath holding were found in almost all of 52 subjects and were regular in a majority. In detailed studies, subjects rebreathed a mixture of 8% CO2 in O2 and then held their breath on an occluded mouthpiece, with glottis open, at functional residual capacity. Contractions monitored as waves of negative pressure were reproducible and increased in amplitude and frequency through the breath hold, but the breakpoint did not always correspond to the same pressure or frequency. Frequency and the time derivative of pressure (dP/dt) of contractions were much higher during breath holding than frequency of breathing and dP/dt of occluded breaths at the same gas tensions during rebreathing. Contractions were reduced in amplitude after the subject took three breaths without altering gas tensions. The results are consistent with the hypothesis that contractions contribute to dyspnea in breath breath holding, but there is not a simple correlation between their magnitude and the degree of dyspnea.

CO2-dependent components of sinus arrhythmia from the start of breath holding in humans

“…At the start of breath holding, when so many of the rhythmic influences on sinus arrhythmia are absent [and when rhythmic negative pressure waves are undetectable (1,32,50,51)], minimal sinus arrhythmia is expected. Yet, all subjects showed substantial sinus arrhythmia from the start of breath holding.…”

“…The central respiratory rhythm is already detectable before the breakpoint of breath holding from inspiratory muscle activity [recorded indirectly from rhythmic waves of negative esophageal pressure and of diaphragmatic electromyogram (EMG) activity recorded across the esophagus (1,32,50,51)]. From these measurements, however, the central respiratory rhythm is not detectable from the start of breath holding.…”

Pathophysiology of obstructive sleep apnoea

“…In another study, involuntary respiratory muscle contractions (recorded as waves of negative pressure) were found in most individuals during breathholding, and increased in amplitude and frequency throughout the breathhold time [190]. The slopes of the pressure waves (dP/dt ) during breathholding were found to be greater than those in the same subjects at the same CO 2 level during rebreathing.…”

“…The slopes of the pressure waves (dP/dt ) during breathholding were found to be greater than those in the same subjects at the same CO 2 level during rebreathing. This suggested that the response is due, in part, to a number of other, possible nonchemical, stimuli [190].…”

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

“…These studies described the cardiovascular response to apnoea as consisting of three distinct phases: (i) a short dynamic phase ( 1), that lasts less than 30 s, characterised by rapid changes in blood Abbreviation: DBP, diastolic blood pressure; fH, heart rate; FIO2, inspired oxygen fraction; MBP, mean blood pressure;Q , cardiac output; SaO2, arterial oxygen saturation; SBP, systolic blood pressure; SV, stroke volume; TPR, total peripheral resistance;V O2, oxygen uptake; 1, first, dynamic phase of the cardiovascular response to apnoea; 2, second, steady-state phase of the cardiovascular response to apnoea; 3, third, dynamic phase of the cardiovascular response to apnoea.pressure and f H ; (ii) a steady state phase ( 2), of about 2 min, in which the values attained by each variable at the end of 1 are maintained invariant; and (iii) a further subsequent dynamic phase ( 3), lasting about 1.5 min, characterised by a continuous decrease in f H and increase in blood pressure, until the volitional breaking point was reached. According to Perini et al (2008Perini et al ( , 2010, the end of 2 might occur at the attainment of the physiological breaking point of apnoea (Hong et al, 1971), which is characterised by a specific alveolar PO 2 and PCO 2 composition possibly capable of inducing the first diaphragmatic contraction (Agostoni, 1963;Cross et al, 2013;Lin et al, 1974;Whitelaw et al, 1981): the higher is the alveolar PO 2 , the higher must be the concomitant PCO 2 eliciting diaphragmatic contractions, and vice versa. Ceteris paribus, the time necessary to reach that alveolar gas composition is directly proportional to the body oxygen stores at the beginning of the apnoea and inversely proportional to the body metabolic rate during apnoea.…”