Effects of sodium bicarbonate ingestion on ventilatory and cerebrovascular responses in resting heated humans.

IF 2.2 3区 医学 Q3 PHYSIOLOGY American journal of physiology. Regulatory, integrative and comparative physiology Pub Date : 2024-10-01 Epub Date: 2024-08-05 DOI:10.1152/ajpregu.00161.2024
Akira Katagiri, Naoto Fujii, Kohei Dobashi, Yin-Feng Lai, Bun Tsuji, Takeshi Nishiyasu
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Abstract

Hyperthermia stimulates ventilation in humans. This hyperthermia-induced hyperventilation may be mediated by the activation of peripheral chemoreceptors implicated in the regulation of respiration in reaction to various chemical stimuli, including reductions in arterial pH. Here, we investigated the hypothesis that during passive heating at rest, the increases in arterial pH achieved with sodium bicarbonate ingestion, which could attenuate peripheral chemoreceptor activity, mitigate hyperthermia-induced hyperventilation. We also assessed the effect of sodium bicarbonate ingestion on cerebral blood flow responses, which are associated with hyperthermia-induced hyperventilation. Twelve healthy men ingested sodium bicarbonate (0.3 g/kg body weight) or sodium chloride (0.208 g/kg). One hundred minutes after the ingestion, the participants were passively heated using hot-water immersion (42°C) combined with a water-perfused suit. Increases in esophageal temperature (an index of core temperature) and minute ventilation (V̇E) during the heating were similar in the two trials. Moreover, when V̇E is expressed as a function of esophageal temperature, there were no between-trial differences in the core temperature threshold for hyperventilation (38.0 ± 0.3 vs. 38.0 ± 0.4°C, P = 0.469) and sensitivity of hyperthermia-induced hyperventilation as assessed by the slope of the core temperature-V̇E relation (13.5 ± 14.2 vs. 15.8 ± 15.5 L/min/°C, P = 0.831). Furthermore, middle cerebral artery mean blood velocity (an index of cerebral blood flow) decreased similarly with heating duration in both trials. These results suggest that sodium bicarbonate ingestion does not mitigate hyperthermia-induced hyperventilation and the reductions in cerebral blood flow index in resting heated humans.NEW & NOTEWORTHY Hyperthermia leads to hyperventilation and associated cerebral hypoperfusion, both of which may impair heat tolerance. This hyperthermia-induced hyperventilation may be mediated by peripheral chemoreceptors, which can be activated by reductions in arterial pH. However, our results suggest that sodium bicarbonate ingestion, which can increase arterial pH, is not an effective intervention in alleviating hyperthermia-induced hyperventilation and cerebral hypoperfusion in resting heated humans.

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摄入碳酸氢钠对静息加热人体通气和脑血管反应的影响。
高热会刺激人体通气。这种由高热引起的过度换气可能是通过激活外周化学感受器介导的,这些化学感受器与呼吸调节有关,可对各种化学刺激(包括动脉 pH 值的降低)做出反应。在此,我们研究了这样一个假设:在静止状态下被动加热时,摄入碳酸氢钠可使动脉 pH 值升高,从而减弱外周化学感受器的活动,缓解热疗引起的换气过度。我们还评估了摄入碳酸氢钠对脑血流反应的影响,脑血流反应与高热引起的换气过度有关。12 名健康男性摄入了碳酸氢钠(0.3 克/千克体重)或氯化钠(0.208 克/千克)。摄入 100 分钟后,参与者被动接受热水浸泡(42°C)和水浸服加热。在两次试验中,加热过程中食管温度(核心温度指数)和分钟通气量(VE)的增加情况相似。此外,当 VE 表示为食管温度的函数时,过度通气的核心温度阈值(37.9 ± 0.3 vs. 38.0 ± 0.4°C,P = 0.338)和核心温度-VE 关系斜率评估的高热诱导过度通气的敏感性(13.7 ± 14.9 vs. 15.8 ± 15.6 L/min/°C,P = 0.748)在两次试验之间没有差异。此外,在这两项试验中,大脑中动脉平均血流速度(脑血流指数)随着加热时间的延长而降低。这些结果表明,摄入碳酸氢钠并不能缓解高热引起的过度通气以及静息加热人体脑血流指数的降低。
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来源期刊
CiteScore
5.30
自引率
3.60%
发文量
145
审稿时长
2 months
期刊介绍: The American Journal of Physiology-Regulatory, Integrative and Comparative Physiology publishes original investigations that illuminate normal or abnormal regulation and integration of physiological mechanisms at all levels of biological organization, ranging from molecules to humans, including clinical investigations. Major areas of emphasis include regulation in genetically modified animals; model organisms; development and tissue plasticity; neurohumoral control of circulation and hypertension; local control of circulation; cardiac and renal integration; thirst and volume, electrolyte homeostasis; glucose homeostasis and energy balance; appetite and obesity; inflammation and cytokines; integrative physiology of pregnancy-parturition-lactation; and thermoregulation and adaptations to exercise and environmental stress.
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