Tsuji Bun, Hoshi Yuta, Honda Yasushi, Fujii Naoto, Sasaki Yosuke, Cheung Stephen S, Kondo Narihiko, Nishiyasu Takeshi
Department of Health Sciences, Prefectural University of Hiroshima, Hiroshima, Japan.
Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba City, Ibaraki, Japan.
Physiol Rep. 2019 Jan;7(1):e13967. doi: 10.14814/phy2.13967.
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 ) reached 39°C or volitional termination. In each trial, participants breathed normally (normal-breathing) or voluntarily controlled minute ventilation (V ) 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 increased as T rose above 38.0 ± 0.3°C, whereas controlled-breathing diminished the increase in V (V at T = 38.6°C: 25.6 ± 5.9 and 11.9 ± 1.3 L min during normal- and controlled-breathing, respectively, P < 0.001). During normal-breathing, end-tidal CO pressure and MCAV decreased with rising T , but controlled-breathing diminished these reductions (at T = 38.6°C, 24.7 ± 5.0 vs. 39.5 ± 2.8 mmHg; 44.9 ± 5.9 vs. 60.2 ± 6.3 cm sec , both P < 0.001). The work of breathing correlated positively with changes in V (P < 0.001) and was lower during controlled- than normal-breathing (16.1 ± 12.6 and 59.4 ± 49.5 J min , 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.
我们研究了热诱导的过度通气是否可以被自主抑制,如果可以,那么在静息状态下受热的人体中,这是如何调节呼吸力学和脑血流量的。在两项独立试验中,10名健康男性通过下半身热水浸泡和覆盖上半身的水灌注衣物(均为41°C)进行被动加热,直至食管温度(T)达到39°C或自主终止。在每项试验中,参与者正常呼吸(正常呼吸组)或自主控制分钟通气量(V),使其达到加热5分钟后观察到的水平(控制呼吸组)。测量呼吸气体、大脑中动脉血流速度(MCAV)、呼吸功以及呼气末和吸气末肺容积。在正常呼吸时,随着T升高至38.0±0.3°C以上,V增加,而控制呼吸减少了V的增加(在T = 38.6°C时,正常呼吸组和控制呼吸组的V分别为25.6±5.9和11.9±1.3 L/min,P < 0.001)。在正常呼吸时,呼气末CO压力和MCAV随着T升高而降低,但控制呼吸减少了这些降低(在T =