Coupling of external to cellular respiration during exercise: the wisdom of the body revisited.

The changes in cellular respiration needed to increase energy output during exercise are intimately and predictably linked to external respiration through the circulation. This review addresses the mechanisms by which lactate accumulation might influence O2 uptake (VO2) and CO2 output (VCO2) kinetics. Respiratory homeostasis (a steady state with respect to VO2 and VCO2) is achieved by 3-4 min for work rates not associated with an increase in arterial lactate. When blood lactate increases significantly above rest for constant work rate exercise, VO2 characteristically increases past 3 min (slow component) at a rate proportional to the lactate concentration increase. The development of a similar slow component in VCO2 is not evident. The divergence of VCO2 from VO2 increase can be accounted for by extra CO2 release from the cell as HCO3- buffers lactic acid. Thus the slow component of aerobic CO2 production (parallel to VO2) is masked by the increase in buffer VCO2. This CO2, and the consumption of extracellular HCO3- by the lactate-producing cells, shifts the oxyhemoglobin dissociation curve rightward (Bohr effect). The exercise lactic acidosis has been observed to occur after the minimal capillary PO2 is reached. Thus the lactic acidosis serves to facilitate oxyhemoglobin dissociation and O2 transport to the muscle cells without a further decrease in end-capillary PO2. From these observations, it is hypothesized that simultaneously measured dynamic changes in VO2 and VCO2 might be useful to infer the aerobic and anaerobic contributions to exercise bioenergetics for a specific work task.