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Aerobically generated CO(2) stored during early exercise.

M L Chuang1, H Ting, T Otsuka

  • 1Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Harbor-University of California Los Angeles Medical Center, Torrance, California 90509, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|September 14, 1999
PubMed
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Early exercise causes metabolic alkalosis in muscles, increasing CO2 stores. This study quantifies this exercise-induced metabolic alkalosis (E-I Alk) component of CO2 stores, finding it

Area of Science:

  • Exercise Physiology
  • Human Metabolism
  • Respiratory Physiology

Background:

  • Muscle metabolic alkalosis occurs during early exercise, linked to phosphocreatine hydrolysis.
  • Femoral vein blood pH, K+, and HCO3- increase without elevated PCO2, indicating CO2 conversion to HCO3- rather than pulmonary elimination.
  • Understanding early CO2 store dynamics is crucial for exercise physiology.

Purpose of the Study:

  • To quantify the increase in early exercise CO2 stores.
  • To determine the specific contribution of exercise-induced metabolic alkalosis (E-I Alk) to these CO2 stores.
  • To investigate the relationship between CO2 kinetics and oxygen uptake during exercise.

Main Methods:

  • Measurements of CO2 stores were conducted at work rates below the lactic acidosis threshold (LAT) to isolate the E-I Alk effect.

Related Experiment Videos

  • The transient increase in CO2 stores was monitored from the airway, starting around 15 seconds into exercise.
  • Analysis included components from the Haldane effect, increased tissue PCO2, and E-I Alk.

    • Main Results:

    • CO2 stores increased significantly within 15 seconds of exercise onset, peaking around 60 seconds and normalizing by 3 minutes.
    • The E-I Alk component constituted a major portion of the increased CO2 stores, averaging 61% at 60% LAT and 68% at 80% LAT.
    • The kinetics of O2 uptake correlated with CO2 store changes, and the O2 deficit correlated with the E-I Alk component.

    Conclusions:

    • A significant portion of the aerobically generated increase in CO2 stores during early exercise is attributed to bicarbonate (HCO3-) produced from phosphocreatine breakdown.
    • Exercise-induced metabolic alkalosis plays a key role in transient CO2 buffering and storage.
    • These findings enhance our understanding of immediate metabolic and respiratory responses to exercise.