CO2 pulse and acid-base status during increasing work rate exercise in health and disease

• Acid–base regulation is shown in one systematic report across a spectrum of diseases.
• We collected acid–base data in various cardiovascular and pulmonary conditions.
• The validity of the anaerobic threshold (AT) measured by gas exchange was confirmed.
• (CO2–O2) pulse difference per heart beat reflected anaerobically-generated excess-CO2.
• Arterial [HCO3−] uniformly correlated with CO2 excess above AT in health and disease.

The CO2 pulse (V˙CO2/heart rate), analogous to the O2 pulse (V˙O2/heart rate), was calculated during cardiopulmonary exercise testing and evaluated in normal and diseased states. Our aim was to define its application in its release in excess of that from V˙CO2/heart rate in the presence of impaired cardiovascular and lung function. In the current study, forty-five patients were divided into six physiological states: normal, exercise-induced myocardial ischemia, chronic heart failure, pulmonary vasculopathy, chronic obstructive pulmonary disease, and interstitial lung disease. We subtracted the O2 pulse from the CO2 pulse to determine the exhaled CO2 that could be attributed to CO2 pulse of buffering of lactic acid. The difference between the CO2 pulse and O2 pulse (V˙CO2/heart rate–V˙O2/heart rate) includes CO2 generated from HCO3− buffering of lactic acid. The accumulated CO2 per body mass was found to be significantly correlated with the corresponding [HCO3−] decrease (R2 = 0.72; P < 0.0001). In summary, the increase in CO2 pulse over the O2 pulse accounted for the anaerobically-generated excess-CO2 in each of the physiological states and correlated with the decreases in the arterial Bicarbonate concentration.