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

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 males (23±2 years) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual's pre-determined peak oxygen uptake (moderate intensity). In order to suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) 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°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°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-1) than at rest (-2±1 L min-1); however, the magnitude of reduction during exercise did not differ at low- (0.5°C) to severe- (2.0°C) increases in esophageal temperature (all P>0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by %change from pre-hyperoxic levels were not different at all levels of hyperthermia (~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.