Ventilatory oscillations at exercise: effects of hyperoxia, hypercapnia, and acetazolamide

Periodic breathing has been found in patients with heart failure and sleep apneas, and in healthy subjects in hypoxia, during sleep and wakefulness, at rest and, recently, at exercise. To unravel the cardiorespiratory parameters liable to modulate the amplitude and period of ventilatory oscillations, 26 healthy subjects were tested under physiological (exercise) and environmental (hypoxia, hyperoxia, hyperoxic hypercapnia) stresses, and under acetazolamide (ACZ) treatment. A fast Fourier transform spectral analysis of breath-by-breath ventilation [Image: see text] evidenced an increase in [Image: see text] peak power under hypercapnia (vs. normoxia and hyperoxia, P < 0.001) and a decrease under ACZ (vs. placebo, P < 0.001), whereas it was not modified in hyperoxia. [Image: see text] period was shortened by exercise in all conditions (vs. rest, P < 0.01) and by hypercapnia (vs. normoxia, P < 0.05) but remained unchanged under ACZ (vs. placebo). [Image: see text] peak power was positively related to cardiac output ([Image: see text]) and [Image: see text] in hyperoxia (P < 0.01), in hypercapnia (P < 0.001) and under ACZ (P < 0.001). [Image: see text] period was negatively related to [Image: see text] and [Image: see text] in hyperoxia (P < 0.01 and P < 0.001, respectively), in hypercapnia (P < 0.05 and P < 0.01, respectively) and under ACZ (P < 0.05 and P < 0.01, respectively). Total respiratory cycle time was the main factor responsible for changes in [Image: see text] period. In conclusion, exercise, hypoxia, and hypercapnia increase ventilatory oscillations by increasing [Image: see text] and [Image: see text], whereas ACZ decreases ventilatory instability in part by a contrasting action on O(2) and CO(2) sensing. An intrinsic oscillator might modulate ventilation through a complex system where peripheral chemoreflex would play a key role.