Relief of the ‘air hunger’ of breathholding. A role for pulmonary stretch receptors

• Published in: Respiration physiology 1996-03, Vol.103 (3), p.221-232
• Main Authors: Flume, Patrick A., Eldridge, Frederic L., Edwards, Lloyd J., Mattison, Lalaine E.
• Format: Article
• Language: English
• Subjects: Adult; Air hunger; Blood Gas Analysis; Breathing; Control of breathing; Female; Forced Expiratory Flow Rates; Heart; Heart Transplantation - physiology; Humans; Lung; Lung Transplantation - physiology; Male; Mammals; Middle Aged; Pulmonary stretch; Pulmonary Stretch Receptors - physiology; Rebreathing; Receptors; Reproducibility of Results; Respiratory; Respiratory Mechanics - physiology; Respiratory sensation; Sensation; Space life sciences; Total Lung Capacity; Transplant; Vagus nerve; Vagus Nerve - physiology
• ISSN: 0034-5687
• DOI: 10.1016/0034-5687(95)00094-1

Fowler (Fowler, W.S., 1954, J. Appl. Physiol. 6:539–545) showed that rebreathing, despite worsening P CO 2 and O 2 saturation, relieved the distress of breathholding; he suggested a role for vagal input in the relief. We studied effects on respiratory sensation of breathholding and rebreathing in normals, patients with bilateral lung transplants (LT), who have a decrease in number of pulmonary stretch receptors (PSR), and heart transplant recipients (HT). Subjects held their breath until distress became intolerable, rebreathed various combinations of CO 2 and O 2, then performed another maximal breathhold. Respiratory distress was rated continuously (visual analog scale) by each subject. Both LT and HT had earlier onset of and more rapidly developing distress during breathholding, resulting in shorter breathhold times, than normals. Relief with rebreathing was neither as rapid nor as great in LT as in HT and normals. Our findings suggest that mechanisms that produce respiratory distress in HT and LT are similar, but differ from normals. However, reduction in distress on rebreathing is more rapid and greater in HT and normals than in LT. This is compatible with the loss during rebreathing of the inhibitory effect of PSR input on neural mechanisms that lead to respiratory distress.