Critical capillary PO2 and the role of lactate production in oxyhemoglobin dissociation during exercise

• Published in: Advances in experimental medicine and biology Vol. 471; p. 321
• Main Author: Wasserman, K
• Format: Journal Article
• Language: English
• Published: United States 1999
• Subjects: Acidosis, Lactic - metabolism; Adult; Blood Gas Analysis; Buffers; Capillaries - metabolism; Cardiac Output, Low - metabolism; Exercise - physiology; Femoral Vein - metabolism; Humans; Lactic Acid - biosynthesis; Oxygen - metabolism; Oxyhemoglobins - metabolism
• ISSN: 0065-2598
• DOI: 10.1007/978-1-4615-4717-4_39

During exercise, O2 transport from capillary to myocyte is not diffusion-limited until end-capillary PO2 reaches its lowest value (critical capillary PO2). Critical capillary PO2 is reached at the mid-level of the subject's work capacity, not at Vo2 max. Femoral vein lactate does not increase until the critical capillary PO2 is reached. The increase in lactate is essential once the critical capillary PO2 is reached because the increase in H+ that accompanies the increase in lactate, through the "Bohr Effect", becomes the mechanism for oxyhemoglobin dissociation. Both normal subjects and patients with chronic stable heart failure have a critical capillary PO2 between 14 and 22 mm Hg. The pattern of femoral vein (end capillary) PO2 change as VO2 increases, describes the Vo2 at which O2 becomes diffusion limited and the extent to which new muscle capillary bed is recruited as Vo2 increases above the lactate threshold.