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 O-2 uptake (Vo(2)) and CO2 output (Vco(2)) kinetics. Respiratory homeostasis (a steady state with respect to Vo(2) and Vco(2)) 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, Vo(2) characteristically increases past 3 min (slow component) at a rate proportional to the lactate concentration increase. The development of a similar slow component in Vco(2) is not evident. The divergence of Vco(2) from Vo(2) increase can be accounted for by extra CO2 released from the cell as HCO3- buffers lactic acid. Thus the slow component of aerobic CO2 production (parallel to Vo(2)) is masked by the increase in buffer Vco(2). 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 Po-2 is reached. Thus the lactic acidosis serves to facilitate oxyhemoglobin dissociation and O-2 transport to the muscle cells without a further decrease in end-capillary Po-2. From these observations, it is hypothesized that simultaneously measured dynamic changes in Vo(2) and Vco(2) might be useful to infer the aerobic and anaerobic contributions to exercise bioenergetics for a specific work task.