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We previously described bicarbonate exchange dynamics in humans at rest and during exercise using a three-compartment model. In the present study we tested the effect of certain assumptions of this model on the prediction of the change in exchangeable bicarbonate with the increased metabolic rate of exercise. We compared this prediction with a measurement of CO2 retention after exercise onset determined from gas exchange data. The change in tissue bicarbonate stores was estimated from differences in the kinetics of adjustment of VO2 and VCO2, and this was added to an estimate of the changes in venous blood gas stores to estimate the total change in bicarbonate. When the commonly held assumption that endogenous CO2 production, thought to occur in a rapidly equilibrating peripheral compartment at rest, was also applied to the exercise condition, the three-compartment bicarbonate model predicted an unphysiologically large increase in bicarbonate stores (700 mmol, or over 15 L). In contrast, the 'gas exchange' approach predicted a relatively small increase in bicarbonate (26 mmol), consistent with other reports. The incompatibility of these findings with the assumption about the source of endogenous CO2 production in the bicarbonate model requires that the underlying physiological correlates of the three compartments change from rest to exercise.

Abstract: A computer model was developed to provide a theoretical framework for interpreting the dynamics of muscle capillary O2 exchange in health and disease. We examined the effects of different muscle oxygen uptake () and CvO2 profiles on muscle blood flow () kinetics (). Further, we simulated and responses to predict the CvO2 profile and the underlying dynamics of capillary O2 exchange (). Exponential equations describing , CvO2 and responses in vivo were used in the simulations. The results indicated that kinetics were relatively insensitive to CvO2 parameters, but directly associated with kinetics. The biphasic response produced a substantial fall in CvO2 within the first 15–20s of the exercise transition (phase 1 of ). These results revealed that the main determinant of CvO2 (or O2 extraction) kinetics was the dynamic interaction of and kinetics during phase 1 of . [Copyright &y& Elsevier]

It has recently been reported that the ‘gain’ of Phase II increase in pulmonary oxygen uptake (i.e. the ‘fundamental’ increase in &Vdot;O2 per unit increase in work rate; Gp) does not attain the anticipated value of ∼10 ml min-1 W-1 following the onset of high-intensity exercise. In the present study, we hypothesised that Gp would fall significantly below 10 ml min-1 W-1 only when the work rate exceeded the so-called ‘critical power’ (CP). Seven healthy males completed several ‘square-wave’ transitions from ‘unloaded’ cycling to work rates requiring 60 and 90% of the gas exchange threshold (GET), 40 and 80% of the difference between the GET and &Vdot;O2 peak (i.e. below and above the CP, respectively), and 100, 110 and 120% of &Vdot;O2 peak. Pulmonary &Vdot;O2 was measured breath-by-breath and &Vdot;O2 kinetics were determined using non-linear regression techniques. The asymptotic Gp was significantly lower at work rates above (7.2–8.6 ml min-1 W-1) compared to work rates below (9.3–9.7 ml min-1 W-1) the CP (P < 0.05). We conclude that the gain of Phase II increase in &Vdot;O2 becomes significantly reduced when the work rate exceeds the CP. [Copyright &y& Elsevier]