Search

New Findings: What is the topic of this review? One of the major unanswered questions in physiology is that of how breathing matches metabolic rate. Venous chemoreceptors seem to have been dismissed since the 1960s. What advances does it highlight? New evidence shows that their apparent dismissal needs reappraisal. The paper on which this depends has more than one interpretation, and another paper obtained the opposite result. Previous search ignored all locations between skeletal muscle and the right heart. Oxygen sensors other than the arterial chemoreceptors do exist. Heymans and colleagues originally demonstrated some residual breathing response to hypoxia in sino-aortically denervated animals. Similar results occur in humans. One of the major unanswered questions in physiology is that of how breathing matches metabolic rate. The existence in humans of venous chemoreceptors that might control breathing seems to have been dismissed since the 1960s. New evidence has emerged showing that this apparent dismissal needs reappraisal. First, the paper in humans on which this depends has more than one interpretation. Moreover, a previous paper obtained the opposite result and is not cited. Secondly, previous search for venous chemoreceptors failed to examine all venous locations between skeletal muscle and the right heart and lungs. Thirdly, oxygen sensors other than the arterial chemoreceptors do exist. Heymans himself originally demonstrated some residual breathing response to hypoxia in sino-aortically denervated animals. Others confirm a residual breathing response to hypoxia in mammals, including humans. There is now considerable interest in the importance of afferent feedback in controlling the cardiovascular and respiratory systems. Moreover, it is now clear that arterial, aortic and central chemoreceptors have no role in explaining how breathing matches metabolic rate during exercise. These together provide a timely reminder that venous chemoreceptors remain ideal candidates still to be considered as metabolic rate sensors to explain matching in humans. Firstly, this is because venous PO2 and PCO2 values do change appropriately in proportion to metabolic rate, so a metabolic rate signal sufficient to drive breathing might already exist. Secondly, chemoreceptor-like anatomical structures are present in the systemic venous system but remain unexplored. Finally, no extant experimental evidence precludes their existence., (© 2017 The Authors. Experimental Physiology © 2017 The Physiological Society.)

Purpose: Contrary to what is commonly assumed, organs continue to move during breath-holding. We investigated the influence of lung volume on motion magnitude during breath-holding and changes in velocity over the duration of breath-holding., Materials and Methods: Sixteen healthy subjects performed 60-second inhalation breath-holds in room-air, with lung volumes of ∼100% and ∼70% of the inspiratory capacity, and exhalation breath-holds, with lung volumes of ∼30% and ∼0% of the inspiratory capacity. During breath-holding, we obtained dynamic single-slice magnetic-resonance images with a time-resolution of 0.6s. We used 2-dimensional image correlation to obtain the diaphragmatic and pancreatic velocity and displacement during breath-holding., Results: Organ velocity was largest in the inferior-superior direction and was greatest during the first 10s of breath-holding, with diaphragm velocities of 0.41mm/s, 0.29mm/s, 0.16mm/s and 0.15mm/s during BH 100% , BH 70% , BH 30% and BH 0% , respectively. Organ motion magnitudes were larger during inhalation breath-holds (diaphragm moved 9.8 and 9.0mm during BH 100% and BH 70% , respectively) than during exhalation breath-holds (5.6 and 4.3mm during BH 30% and BH 0% , respectively)., Conclusion: Using exhalation breath-holds rather than inhalation breath-holds and delaying irradiation until after the first 10s of breath-holding may be advantageous for irradiation of abdominal tumors., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

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.

Objective: The etiology of oligohydramnios-related pulmonary hypoplasia is not understood but is known to involve chronic lung liquid loss. We tested the hypothesis that low amniotic pressure in oligohydramnios disturbs the normal tracheal-amniotic pressure gradient to increase lung liquid loss and impair lung development., Study Design: Chronic pharyngeal catheterization with drainage to the exterior was used in 15 fetal sheep to mimic reduced amniotic pressure at the upper airway in the presence of normal amniotic fluid volume., Results: Pharyngeal pressures relative to amniotic pressures were negative in all drained fetuses (mean +/- SE -3.0 +/- 0.6 mm Hg), in contrast to positive pressures in controls (0.7 +/- 0.1 mm Hg). There was no significant difference in lung weight or deoxyribonucleic acid relative to body weight, or in lung morphometry, between 10 fetuses drained for 10 to 21 days and their control cotwins., Conclusion: Mimicking low amniotic pressure in the upper airway by chronic fetal pharyngeal drainage does not impair lung development in fetal sheep.

The mechanism of oligohydramnios-related pulmonary hypoplasia (PH) is not understood, but is known to involve chronic loss of lung liquid. In order to investigate the recent suggestion that fetal breathing movements are absent or diminished in oligohydramnios-related PH, we made continuous recordings of fetal breathing movements (FBM) during chronic lung drainage in tracheostomized fetal sheep. FBM remained present throughout the drainage period. There was no significant difference in the number or duration of FBM epochs in tracheostomized fetuses compared to controls, although there was a slight reduction in incidence between 126 and 133 days (P = 0.02). PH in the fetuses undergoing chronic lung liquid drainage was confirmed by significant reductions in lung weight, volume, DNA, and total airspace, and in altered maturation. This study is consistent with other data suggesting that inhibition of FBM is not the primary mechanism of oligohydramnios-related pulmonary hypoplasia.