COMPUTER-SIMULATION OF O2 TRANSPORT AND UTILIZATION MECHANISMS AT THE ONSET OF EXERCISE

During transitions in work rate, O2 uptake (VO2) kinetics at the working tissue level might be rate limited by O2 transport and/or by O2 utilization. A computer model with parallel working and non-working tissue compartments, connected to an ideal lung by a variable-sized venous blood volume, was developed to study this. The time constant for working tissue O2 demand (tau(T)) was set by a first-order linear metabolic response. The model attempted to replicate the VO2 response at the alveolar level of a single subject performing step transitions on a cycle ergometer from 25 to 105 W [total lag time (equivalent to 63% increase above baseline) = 40.2 s]. Measured cardiac output kinetics (total lag time = 44.1 s) were used as a model parameter. Blood flow to the nonworking tissue (QNW) was kept constant at 4.5 or 5.0 l/min. A critical PO2 of 20 Torr was set, and the Bohr effect on the O2-hemoglobin dissociation curve was included. The ''best'' simulation had tau(T) = 36 s, QNW = 4.5 l/min, and venous blood volume = 2 liters and was not 02 transport limited. The approximation to the real data was good in all but the phase 1 response, where the model underpredicted the measured response. However, when QNW was increased to 5.0 l/min, the model was O2 transport limited; yet the predicted VO2 response at the alveolar level was not notably different from the subject's data. The model has predicted that the system works at or near the O2 transport limitation condition with a high sensitivity to changes in blood flow and position of the O2-hemoglobin dissociation curve.