title: Ventilatory regulation of arterial H(+) (pH) during exercise.
abstract: We hypothesized that exercise ventilation and arterial H(+) ([H(+)]a) are mutually interactive, [H(+)]a stimulating V(E) and V(E) regulating [H(+)]a increase. Fifty-five patients were studied, 10 normal and 45 with cardio-respiratory disorders. Each patient underwent cardiopulmonary exercise testing with simultaneous serial arterial blood gas and pH measurements. Subsequently, they were classified into one of 7 clinical groups: (1) normal, (2) exercise-induced hypoxemia (PaO2<50mmHg), (3) exercise-induced myocardial ischemia, (4) heart failure, (5) COPD, (6) interstitial lung disease, and (7) pulmonary vasculopathy. The average resting pHa was 7.42 or 7.43 for each group. At anaerobic (lactic acidosis) threshold (AT), [H(+)]a increased due to PaCO2 increase (+2mmHg), primarily. At peak exercise, [H(+)]a increased further due to arterial HCO3(-) decrease. In summary, [H(+)]a appears to be closely regulated at rest to AT and further to peak exercise by CO2 elimination from the venous return. No evidence was observed for over-ventilation of CO2, causing the arterial blood to become more alkaline during exercise in the patient groups studied.
authors.affiliation: Division of Respiratory and Critical Care, Physiology and Medicine, Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, David Geffen School of Medicine, University of California at Los Angeles, Torrance, CA 90502, United States. Electronic address: kwasserman@LABiomed.org.
authors.forename: Karlman
authors.initials: K
authors.lastname: Wasserman
authors.affiliation: Division of Respiratory and Critical Care, Physiology and Medicine, Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, David Geffen School of Medicine, University of California at Los Angeles, Torrance, CA 90502, United States.
authors.forename: Timothy A
authors.initials: TA
authors.lastname: Cox
authors.affiliation: Division of Respiratory and Critical Care, Physiology and Medicine, Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, David Geffen School of Medicine, University of California at Los Angeles, Torrance, CA 90502, United States.
authors.forename: Kathy E
authors.initials: KE
authors.lastname: Sietsema
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology*; D000328:Adult; D000368:Aged; D001784:Blood Gas Analysis; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008171:Lung Diseases / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery / Q000378:metabolism*; D011659:Pulmonary Gas Exchange; D012123:Pulmonary Ventilation / Q000502:physiology; D012119:Respiration; D013997:Time Factors; D055815:Young Adult
keywords: Acid–base regulation; Arterial pH; Exercise; Hypoxemia; Physiological dead space/tidal volume ratio; Ventilation–arterial H(+) interaction