Open AccessRespiratory mechanics and cerebral blood flow during heat‐induced hyperventilation and its voluntary suppression in passively heated humans
Author(s) -
Tsuji Bun,
Hoshi Yuta,
Honda Yasushi,
Fujii Naoto,
Sasaki Yosuke,
Cheung Stephen S.,
Kondo Narihiko,
Nishiyasu Takeshi
Publication year - 2019
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13967
Subject(s) - hyperventilation , medicine , work of breathing , anesthesia , ventilation (architecture) , breathing , respiratory physiology , respiratory system , cerebral blood flow , tidal volume , respiratory rate , cardiology , blood pressure , heart rate , physics , thermodynamics
We investigated whether heat‐induced hyperventilation can be voluntarily prevented, and, if so, how this modulates respiratory mechanics and cerebral blood flow in resting heated humans. In two separate trials, 10 healthy men were passively heated using lower body hot‐water immersion and a water‐perfused garment covering their upper body (both 41°C) until esophageal temperature ( T es ) reached 39°C or volitional termination. In each trial, participants breathed normally (normal‐breathing) or voluntarily controlled minute ventilation ( V E ) at a level equivalent to that observed after 5 min of heating (controlled‐breathing). Respiratory gases, middle cerebral artery blood velocity (MCAV), work of breathing, and end‐expiratory and inspiratory lung volumes were measured. During normal‐breathing, V E increased as T es rose above 38.0 ± 0.3°C, whereas controlled‐breathing diminished the increase in V E ( V E at T es = 38.6°C: 25.6 ± 5.9 and 11.9 ± 1.3 L min −1 during normal‐ and controlled‐breathing, respectively, P < 0.001). During normal‐breathing, end‐tidal CO 2 pressure and MCAV decreased with rising T es , but controlled‐breathing diminished these reductions (at T es = 38.6°C, 24.7 ± 5.0 vs. 39.5 ± 2.8 mmHg; 44.9 ± 5.9 vs. 60.2 ± 6.3 cm sec −1 , both P < 0.001). The work of breathing correlated positively with changes in V E ( P < 0.001) and was lower during controlled‐ than normal‐breathing (16.1 ± 12.6 and 59.4 ± 49.5 J min −1 , respectively, at heating termination, P = 0.013). End‐expiratory and inspiratory lung volumes did not differ between trials ( P = 0.25 and 0.71, respectively). These results suggest that during passive heating at rest, heat‐induced hyperventilation increases the work of breathing without affecting end‐expiratory lung volume, and that voluntary control of breathing can nearly abolish this hyperventilation, thereby diminishing hypocapnia, cerebral hypoperfusion, and increased work of breathing.