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Extra info for Pulmonary Manifestations of Rheumatic Disease, An Issue of Clinics in Chest Medicine (The Clinics: Internal Medicine)
Pyruvate concentration, on the other hand, actually increases more rapidly at the start of recovery (see Fig. 14, middle panel). Thus, as soon as exercise stops (and the O2 requirement decreases), the L/P ratio reverses, supporting the evidence obtained during exercise that the exercise-induced lactate increase is not simply a mass action effect consequent to pyruvate increase. 142 In summary, it is difficult to attribute the increase in lactate with an increase in L/P ratio, as seen with heavy exercise, solely to accelerated glycolysis, inadequate tricarboxylic acid cycle enzymes, or changes in contracting muscle fiber type.
This reaction produces new HCO −3 buffer. 0 mmol/L. 147 This early exercise-induced metabolic alkalosis masks the initial metabolic acidosis caused by the increase in lactate. , the V˙O2 above which there is a sustained lactate increase) slightly precedes the decrease in arterial Std HCO −3. 125 The LAT contrasts with the LT in methodology only. The latter is determined from actual measurements of arterial lactate increase, whereas the former is determined by the decrease in arterial HCO −3 concentration due to its buffering of newly accumulating lactic acid.
12. In this plot, the data points are distributed with the same deviation relative to the average curve as they were distributed in the individual curves for each subject. 5 mmol/L. 12 (upper panel), a monoexponential model of lactate increase from rest as a function of V˙O2 does not describe the lactate data well. Lactate points fall above the model curve at the low V˙O2 values, whereas in the region of V˙O2 just below that at which lactate starts to rise (identified as the threshold in the threshold model), the points fall below the model curve.