Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans

被引:12
作者
Fujii, Naoto [1 ]
Kashihara, Miki [1 ]
Kenny, Glen P. [2 ]
Honda, Yasushi [1 ]
Fujimoto, Tomomi [1 ]
Cao, Yinhang [1 ]
Nishiyasu, Takeshi [1 ]
机构
[1] Univ Tsukuba, Fac Hlth & Sport Sci, Tsukuba, Ibaraki 3058574, Japan
[2] Univ Ottawa, Human & Environm Physiol Res Unit, Ottawa, ON, Canada
关键词
heat stroke; peripheral chemoreceptors; respiratory alkalosis; selective brain cooling; CEREBRAL-BLOOD-FLOW; CORE TEMPERATURE THRESHOLDS; SYMPATHETIC-NERVE ACTIVITY; BODY-TEMPERATURE; HEAT-STRESS; VENTILATORY RESPONSE; PASSIVE HYPERTHERMIA; CARBON-DIOXIDE; CHEMOREFLEXES; RESPIRATION;
D O I
10.1152/japplphysiol.00562.2018
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (-9 to -13 l/min) than at rest (-2 +/- 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5 degrees C) to severe (2.0 degrees C) increases in esophageal temperature (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.
引用
收藏
页码:305 / 313
页数:9
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