Respiratory mechanics and cerebral blood flow during heat-induced hyperventilation and its voluntary suppression in passively heated humans.

Bun Tsuji,Takeshi Nishiyasu,Yasushi Honda,Naoto Fujii,Yuta Hoshi,Narihiko Kondo,Yosuke Sasaki,Stephen S Cheung

doi:10.14814/phy2.13967

Abstract

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 CO2 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.

Highlights

Hyperthermia is known to cause cerebral hypoperfusion at rest (Fan et al 2008; Fujii et al 2008a; Low et al 2008; Brothers et al 2009; Nelson et al 2011) and during exercise (Nybo and Nielsen 2001; Hayashi et al 2011)
This study examined whether heat-induced hyperventilation can be diminished through voluntary control of breathing, and, if so, how this affects respiratory mechanics, PaCO2, and middle cerebral artery blood velocity (MCAV) during passive heating
This spontaneous hyperventilation elicited by passive heating can be nearly prevented by voluntary control of breathing, which attenuated largely the decreases in PETCO2 and MCAV

Summary

Introduction

Hyperthermia is known to cause cerebral hypoperfusion at rest (Fan et al 2008; Fujii et al 2008a; Low et al 2008; Brothers et al 2009; Nelson et al 2011) and during exercise (Nybo and Nielsen 2001; Hayashi et al 2011). This effect may cause elevations in brain temperature (Nybo et al 2002) and central fatigue (Ross et al 2012), which could contribute to the development of heat-related illness and to decreased exercise performance in the heat.

Results

Discussion

Conclusion