Arterial CO2 Pressure Drives Ventilation with a Time Delay during Recovery from an Impulse-like Exercise without Metabolic Acidosis

We investigated this hypothesis that arterial CO2 pressure (PaCO2) drives ventilation (V . E) with a time delay during recovery from short impulse-like exercise (10 s) with work load of 200 watts. V . E and end tidal CO2 pressure (PETCO2) were measured continuously during rest, warming up, exercise and recovery periods. PaCO2 was predicted (PaCO2 pre) from PETCO2 and tidal volume (VT). PETCO2 and PaCO2 pre peaked at 20 s of recovery. V . E increased and peaked at the end of exercise and then decreased during recovery; however, it peaked again at 30 s of recovery, which was 10 s later than the peak of PaCO2 pre. The relationship between V . E and PaCO2pre was not significant by using data of them obtained at the same time but was significant by using data of V . E obtained 10 s later for data of PaCO2 pre. The results support our hypothesis that PaCO2 drives V . E with a time delay. Keywords—Arterial CO2 pressure, impulse-like exercise, time delay, ventilation.