Ventilatory Responses During Ramp Exercise in Hyperoxia

Abstract

Hyperpnea during heavy exercise is generally thought to be closely coupled with the onset of anaerobic metabolism. Arterial acidosis stimulates the carotid chemoreceptors and the resultant hyperpnea produces arterial hypocapnia. This is supported by the finding that the asthmatic patients with carotid body resection do not hyperventilate during heavy exercise [14]. However, several investigators who have studied human subjects with dietary glycogen depletion have suggested a dissociation of hyperventilation and lactic acid production [7]. In ponies, significant arterial hypocapnia is always observed even during mild to moderate exercise and carotid body denervation accentuates rather than attenuates the hypocapnia during heavy exercise [11,12]. This group has claimed that hyperpnea during heavy exercise is not tightly dependent on arterial acidosis and that the carotid chemoreceptors contribute minimally to hyperventilation not only in ponies but also in humans [5]. The present study was undertaken to assess the role of the carotid chemoreceptors during incremental exercise in healthy human subjects. Carotid body sensitivity to humoral stimuli such as H⁺, K⁺, and plasma catecholamines is believed to be attenuated significantly by breathing an O₂-rich gas mixture [1,3]. Assuming that the nonlinear increase of the $\dot V$E response during incremental ramp exercise is primarily dependent on the ventilatory drive mediated by the carotid bodies, hyperoxia would diminish hyperventilation during heavy exercise. Furthermore, as sustained hyperoxia has been shown to significantly reduce the blood lactate level during heavy exercise [13,15], bicarbonate buffering and the resultant production of extra CO₂ would disappear or would appear at a higher work rate when O₂ rich-gases are inhaled.