Do Carotid Chemoreceptors Contribute to Hyperthermia Induced Hyperventilation in Exercising Humans?

Abstract

Hyperthermia increases ventilation in resting and exercising humans (White, J Appl Physiol 101: 655–663, 2006; Fujii et al. J Appl Physiol 104:998–1005, 2008), though what mechanisms mediate this response remains unclear. Carotid chemoreceptors can contribute to ventilatory regulation. Since hyperthermia can augment carotid chemoreceptor activity as demonstrated under in vitro conditions (Eyzaguirre and Zapata, J Appl Physiol 57: 931–957, 1984), this increased activity may in part mediate hyperthermia induced hyperventilation in humans. Regarding this, we previously reported that carotid chemoreceptor is not a main factor mediating hyperthermia induced hyperventilation at rest (Fujii et al. Exp Physiol 93: 994–1001, 2008). However, given hyperthermia induced hyperventilation differs between rest and exercise (Fujii et al. J Appl Physiol 104:998–1005, 2008), the results obtained at rest may not be representative of the response in exercise. Therefore, the purpose of this study was to evaluate whether carotid chemoreceptors contribute to hyperthermia‐induced hyperventilation in exercising humans. Eleven healthy young males (21 ± 3 years) performed cycling in the heat (37 °C) (35–55 min) at a fixed submaximal workload equal to ~55% of the individual's pre‐determined peak oxygen uptake. In order to suppress carotid chemoreceptor activity, 30‐s hyperoxic breathing (100% O2) was performed at rest (before exercise), 5 min into exercise, as well as at increasing levels of hyperthermia as defined by an increase in esophageal temperature (an index of body core temperature) of 0.5, 1.0, and 1.5 °C above levels measured at 5‐min into exercise. Ventilation during exercise gradually increased as esophageal temperature increased (all P < 0.05), indicating that hyperthermia induced hyperventilation occurred. Carotid chemoreceptor inhibition with hyperoxic breathing suppressed ventilation at rest as well as during exercise regardless of the level of hyperthermia (all P < 0.05). Hyperoxia induced changes in ventilation (as assessed by % change from pre‐hyperoxic level) were −15 ± 7 % at rest and −15 ± 6 % at 5 min into exercise. The hyperoxia induced changes in ventilation during exercise for an esophageal temperature increase of 0.5, 1.0, and 1.5 °C were −18 ± 7 %, −17 ± 7 %, and −19 ± 8 %, all of which were not different from the 5‐min exercise level (all P > 0.05). These results demonstrate that carotid chemoreceptor contribution to ventilation during exercise is not modulated by the level of hyperthermia. Thus, we show that carotid chemoreceptors are not largely involved in the regulation of hyperthermia induced hyperventilation in exercising humans irrespective of state of hyperthermia.Support or Funding InformationThis study was supported by the grants from Ministry of Education, Culture, Sports, Science and Technology in Japan and Japan Society for the Promotion of Science.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.