Carotid body hyperexcitability underlies heat-induced hyperventilation in exercising humans

Physical activity is the most common source of heat strain for humans. The thermal strain of physical activity causes overbreathing (hyperventilation) and this has adverse physiological repercussions. The mechanisms underlying heat-induced hyperventilation during exercise are unknown, but recent evidence supports a primary role of carotid body hyperexcitability (increased tonic activity and sensitivity) underpinning hyperventilation in passively heated humans. In a repeated-measures crossover design, 12 healthy participants (6 female) completed two low-intensity cycling exercise conditions (25% maximal aerobic power) in randomized order, one with core temperature (T ) kept relatively stable near thermoneutrality, and the other with progressive heat strain to +2°C T . To provide a complete examination of carotid body function under graded heat strain, carotid body tonic activity was assessed indirectly by transient hyperoxia, and its sensitivity estimated by responses to both isocapnic and poikilocapnic hypoxia. Carotid body tonic activity was increased by 220 ± 110% during cycling alone, and by 400 ± 290% with supplemental thermal strain to +1°C T , and 600 ± 290% at +2°C T (interaction, = 0.0031). During exercise with heat stress at both +1°C and +2°C T , carotid body suppression by hyperoxia decreased ventilation below the rates observed during exercise without heat stress ( < 0.0147). Carotid body sensitivity was increased by up to 230 ± 190% with exercise alone, and by 290 ± 250% with supplemental heating to +1°C T and 510 ± 470% at +2°C T (interaction, = 0.0012). These data indicate that the carotid body is further activated and sensitized by heat strain during exercise and this largely explains the added drive to breathe. Physical activity is the most common way humans increase their core temperature, and excess breathing in the heat can limit heat tolerance and performance, and may increase the risk of heat-related injury. Dose-dependent increases in carotid body tonic activity and sensitivity with core heating provide compelling evidence that carotid body hyperexcitability is the primary cause of heat-induced hyperventilation during exercise.