Quantifying Ventilatory Control with 3% CO2 Inhalation During Exercise

Suhaib Mustafa Hashem ^1* Stanley Yamashiro ¹ Takahide Kato ² Takaaki Matsumoto ³ Vasilis Z Marmarelis ¹

• ¹ University of Southern California, Los Angeles, United States
• ² Toyota National College of Technology, Toyota, Aichi, Japan
• ³ Graduate School of Health and Sport Sciences, Chukyo University, Toyota, Aichi, Japan

Introduction: CO2 mediated ventilation is mainly controlled by two homeostatic mechanisms.The central chemoreceptors are slower mechanisms that focus on blood pH sensing in the brain stem while the peripheral chemoreceptors are quicker to respond and reside in the carotid bodies.Quantification of these mechanisms in humans remain debated.Objective: To quantify the impact that the central and peripheral chemoreceptors have on ventilation in response to changes in PETCO2 during exercise with normoxic breathing and 3% CO2 inhalation.Method: Six healthy males participated in a 5-stage bike protocol with and without 3% CO2 inhalation. We analyzed the time series data of their breath-by-breath PETCO2 and ventilation and generated a one inputone output model via the Laguerre expansion technique (LET) to construct the gain function and quantify the low (0.002 to 0.029 Hz) and high (0.03 to 0.15 Hz) frequency components using the weighted gain averages (WGA) as estimators of central and peripheral chemoreflex mechanisms respectively.Results: 3% CO2 inhalation caused a significant increase the high frequency WGAs at rest and in all levels of exercise except heavy exercise. The low frequency WGAs, however, only maintain significance during rest and the baseline session of exercise.Changes in WGA can be used as quantitative estimates of central and peripheral chemoreflexes. 3% CO2 activates both reflexes and is more apparent in the higher frequency WGAs during exercise due to the oxygen dependent mechanisms effects of exercise.