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

Nevner hvordan økt CO2 korrelerer med økt pustefrekvens under kort, intens intervalltrening.

Abstract—We investigated this hypothesis that arterial CO2 pressure (PaCO2) drives ventilation (VE) with a time delay during recovery from short impulse-like exercise (10 s) with work load of 200 watts. VE 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. VE 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 VE and PaCO2pre was not significant by using data of them obtained at the same time but was significant by using data of VE obtained 10 s later for data of PaCO2 pre. The results support our hypothesis that PaCO2 drives VE with a time delay.

VE started to increase and peaked once again at 30 s of recovery, which was 10 s later than the peaks of PETCO2 and PaCO2 pre (20 s of recovery).Thus, this further drive and the second peak of VE might be attributed to PaCO2. It is known that carotid bodies respond to hypercapnia [15], and central chemoreceptors would be stimulated more by hypercapnia than by acute metabolic acidosis of arterial blood because the blood-brain barrier is relatively impermeable to H+ but is permeable to CO2 [16].

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