This study was done to address the question as to whether there was an exercise metabolic rate below which the O2 supply to the muscles was adequate to meet the O2 requirement and above which the O2 supply was inadequate, ie, an anaerobic threshold (AT). The question was addressed using 2 approaches: (1) The arterial lactate/pyruvate ratio was measured to see if it increased at an O2 uptake (VO2) threshold or continuously as a log function over the entire range of exercise work rates. (2) Anticipating that the VO2 would be affected by reducing O2 supply only for work rates above the AT, the effect of reducing O2 delivery on VO2 for work rates over the entire range of the subject's work capacity was determined. Lactate (L) and pyruvate (P) were measured in arterial blood in 10 normal subjects. The L/P ratio was found not to increase until a threshold work rate was reached, the VO2 being that identified as the AT. Above that VO2, the L/P ratio climbed steeply. Arterial L/P ratio measurements fit a threshold model considerably better than a continuous model, supporting the concept that exercise done at low and moderate work rates can be performed without a change in cell redox state; but redox state does change rapidly in relation to the work rate increase above the AT. In the second study, the cardiorespiratory responses to various levels of exercise were studied in 10 normal subjects before and after carboxyhemoglobin (COHb) was increased to 10% and 20%. The lactic acidosis threshold and VO2 kinetics were examined. Blood lactate concentration increased only above the AT. The AT was systematically decreased by the percent of COHb increase. Importantly, VO2 was reduced and VO2 kinetics were slowed in response to exercise only for the metabolic rates above the AT. These studies demonstrate that lactate increase in response to exercise is O2 flow sensitive, and there is a threshold work rate above which this sensitivity becomes manifest.