William L. Beaver

Mechanisms and patterns of blood lactate increase during exercise in man.

The close balance between the O2 requirement to perform exercise and the O2 supply was analyzed. A non-uniform capillary PO2 can result in anaerobic metabolism in some muscle fibers despite an apparently adequate mean capillary PO2. The pattern of lactate increase for constant work rates and incremental exercise is described. Lactate increases without an increase in pyruvate at a threshold work rate above which the lactate/pyruvate ratio increases. The latter decreases immediately at the start to recovery. From simultaneous measurements of arterial lactate and pyruvate during exercise and recovery, we conclude that the lactate increase at the lactate threshold is consequent to a change in redox state rather than a mass action effect.

Muscle RQ and Lactate Accumulation from Analysis of the VCo2-Vo2Relationship During Exercise

We analyzed the Vco2-Vo2 relationship derived from 1-min incremental (15 W/min) exercise tests of 10 normal subjects. The curve was quite linear below the anaerobic threshold (AT). We deduce that the slope must equal the respiratory quotient (RQ) of the exercising muscles, with a mean value for these subjects of 0.97‡0.06, indicating that the metabolic substrate is essentially glycogen. Beyond the AT, respiratory CO2 output rises at a faster rate above as compared to below the AT, reflecting the rate of HCO3-buffering of lactic acid. Projecting the straight line of Vco2 versus Vo2 below the AT into the region beyond the AT provides an estimate of the Vco2 due to continuing aerobic metabolism. The difference between the actual Vco2 and the aerobically produced Vco2 (excess Vco2) describes the rate of CO2 generated from HCO3- buffering of lactic acid. The integrated excess CO2, corrected for any hyperventilation, provides a measure of the quantity of HCO3- depletion and thus lactate accumulation. Since our measurements are non-steady state, a dynamic simulation model of total lactate accumulation and arterial lactate concentration, based on excess CO2 output and compartmental blood flows and volumes, was developed and found to predict experimental results of lactate concentration increase. Thus, the excess CO2 output can be a useful measure of lactate accumulation and, with the developed model, serve to describe the rise in arterial lactate concentration during a progressively increasing work rate test.

Arterial H+ regulation during exercise in humans

Resting arterial H+ concentration ([H+]a) is in the nanomolar range (40±2 nm/L) while its production is in the millimolar range/min, with little variation from subject to subject. To determine the precision with which [H(+)]a is regulated during exercise, [H+]a, PaCO2 and ventilation (V˙(E)) were measured during progressively increasing work rate exercise in 16 normal subjects. (V˙(E)) increased with [H+]a, the latter attributable to PaCO2 increase below the lactic acidosis threshold (LAT) (ΔV˙(E)/Δ[H+]a ≈ 15   L   min(-1)   nanomol(-1)). [H+]a and PaCO2 increased, simultaneously, as work rate was increased below LAT. PaCO2 reversed direction of change between LAT and ventilatory compensation point (VCP). Above LAT, [H+]a increase relative to (V˙(E)) increase was greater than below LAT. PaCO2 decreased above the LAT, while [H+]a continued to increase. Thus the exercise acidosis was converted from respiratory, below, to a metabolic, above the LAT. We conclude that [H+]a is increased and regulated over the full range of exercise, but with less sensitivity above the LAT.