Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans
Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans
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DOI：
10.1152/japplphysiol.00562.2018
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发表时间：
2019-02-01
影响因子：
3.3
通讯作者：
Nishiyasu, Takeshi
中科院分区：
文献类型：
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作者：
Fujii, Naoto;Kashihara, Miki;Nishiyasu, Takeshi
体温过高会导致休息时和运动时的过度换气。我们以前报道，颈动脉化学感受器部分有助于高血压引起的过度通气在休息。然而，考虑到高血压引起的过度换气在休息和运动之间有显著差异，在休息时获得的结果可能不能代表运动中的反应。因此，我们评估颈动脉化学感受器是否有助于高血压引起的过度换气运动的人。11名健康的年轻男性（23 +/- 2岁）骑自行车在节拍（37摄氏度）在一个固定的次最大的工作量等于类似于55%的个人的预定峰值摄氧量（中等强度）。抑制颈动脉化学感受器的活动。在静息状态（运动前）和运动过程中进行30 s高氧呼吸（100% O-2），体温升高水平定义为食管温度升高0.5 ℃（低）、1.0 ℃（中度）、1.5 ℃（高）和2.0 ℃（重度）。随着食管温度的升高，运动时通气量逐渐增加（均P0.05）.同样地，在运动期间，高氧诱导的通气变化（通过相对于高氧前水平的百分比变化评估）在所有高温水平下均无差异（类似于15- 20%，均P > 0.05）。我们发现，在年轻男性颈动脉化学感受器的贡献hyperthrombia引起的过度通气是相对较小的低至严重的增加，在身体核心温度引起的中等强度的运动在热。新的和值得注意的是，运动引起的增加，在高温导致一个渐进的增加，在人类的通气。然而.这一对策所依据的机制仍未得到解决。我们发现，在年轻男性中，与运动诱导的体温过高相关的过度通气主要不是由颈动脉化学感受器介导的。这项研究提供了重要的新的见解的机制（S）的基础上的调节高血压诱导的过度通气在人类和表明，因子（S）以外的颈动脉化学感受器在介导这种反应中发挥更重要的作用。
Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 +/- 2 yr) cycled in the beat (37 degrees C) at a fixed submaximal workload equal to similar to 55% of the individual's predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity. 30-s hyperoxia breathing (100% O-2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5 degrees C (low), 1.0 degrees C (moderate), 1.5 degrees C (high), and 2.0 degrees C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (similar to 15-20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat.NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However. the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.