Tight coupling between inspiration and expiration after the respiratory compensation point

Background: The respiratory compensation point (RCP) is the point at which arterial PCO 2 starts to decline during heavy exercise. It has been interpreted as a ventilatory response to lactic acidosis. However, in incremental exercise-- there is often a delay between the onset of lactic acidosis and the RCP, which has been ascribed to buffering of the acid. Question: can analysis of respiratory variability provide more insight into the underlying mechanism? Methods: Ten healthy subjects underwent a maximal incremental cycling test. In nine subjects, an RCP was identified as the start of a decline in mean expiratory PCO 2 . Breath-to-breath variability of tidal volume (VT), inspiratory and expiratory time (TI and TE) were analysed with spectral analysis. Results: After the RCP, TI and TE became almost equal to each other (TE – TI = 0.01 ± 0.01 s, mean ± SD, after low-pass filtering). Subsequently, both TI and TE decreased linearly as a function of time (average r 2 > 0.90). The variability of TI and TE decreased by 0.76 ± 0.19 and 0.99 ± 0.31 (expressed as logarithmic power; P 0.99 (for low frequencies). The gain from TI to TE decreased to 1.06 ± 0.106, meaning that changes in TI became virtually equal to changes in TE. Conclusion: After the RCP, a strong linear relation develops between TI and TE, while their variability decreases. The tight respiratory timing during heavy exercise is possibly explained by the action of the lung inflation reflex (Hering-Breuer), in a situation in which both the end-inspiratory lung volume and the respiratory drive are high.