Gas exchange theory and the lactic acidosis (anaerobic) threshold.
The physiological requirements of performing exercise above the anaerobic threshold are considerably more demanding than for lower work rates. Lactic acidosis develops at a metabolic rate that is specific to the individual and the task being performed. Although numerous pyruvate-dependent mechanisms can lead to an elevated blood lactate, the increase in lactate during muscular exercise is accompanied by an increase in lactate/pyruvate ratio (i.e., increased NADH/NAD ratio). This is typically caused by an inadequate O2 supply to the mitochondria. Thus, the anaerobic threshold can be considered to be an important assessment of the ability of the cardiovascular system to supply O2 at a rate adequate to prevent muscle anaerobiosis during exercise testing. In this paper, we demonstrate, with statistical justification, that the pattern of arterial lactate and lactate/pyruvate ratio increase during exercise evidences threshold dynamics rather than the continuous exponential increase proposed by some investigators. The pattern of change in arterial bicarbonate (HCO3-) and pulmonary gas exchange supports this threshold concept. To estimate the anaerobic threshold by gas exchange methods, we measure CO2 output (VCO2) as a continuous function of O2 uptake (VO2) (V-slope analysis) as work rate is increased. The break-point in this plot reflects the obligate buffering of increasing lactic acid production by HCO3-. The anaerobic threshold measured by the V-slope analysis appears to be a sensitive index of the development of metabolic acidosis even in subjects in whom other gas exchange indexes are insensitive, owing to irregular breathing, reduced chemoreceptor sensitivity, impaired respiratory mechanics, or all of these occurrences.
Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance 90509.
K
K
Wasserman
W L
WL
Beaver
B J
BJ
Whipp
D000140:Acidosis, Lactic / Q000209:etiology*; D015308:Anaerobic Threshold / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D010101:Oxygen Consumption; D011659:Pulmonary Gas Exchange / Q000502:physiology*; D011773:Pyruvates / Q000097:blood; D019289:Pyruvic Acid
D011773:Pyruvates; D019289:Pyruvic Acid